Effect of transcutaneous electrical acupuncture point stimulation on expression of p-JNK in the dorsal root ganglion in a rat model of myofascial pain syndrome.

BACKGROUND: Acupuncture has been used to treat myofascial pain syndrome (MPS) for 2000 years in China, but its mechanisms are still not entirely clear. In the present study, we explored the effects of transcutaneous electrical acupuncture point stimulation (TEAS) at an Ashi acupuncture point on expression of phosphorylated c-Jun N-terminal kinase (p-JNK) in the dorsal root ganglion (DRG) using a rat model of MPS. METHODS: 32 rats were divided into four groups: normal, MPS, MPS+TEAS and MPS+sham- TEAS. MPS was produced by a blunt strike to the left vastus medialis combined with eccentric exercise for 8 weeks. Rats in the MPS+TEAS group received TEAS (6-9 mA, 2 Hz, 30 min) treatment at the Ashi acupuncture point for 2 weeks; rats in the MPS+sham -TEAS group had the same electrodes applied but received no stimulation. Paw withdrawal thermal latency (PWTL) was studied at baseline and on days 3, 7, 11 and 15 after treatment. Haematoxylin and eosin staining was used to examine for morphological changes in the left vastus medialis muscles; expression of p-JNK in the L3-L5 DRG was determined by immunofluorescence staining and western blotting after treatment. RESULTS: Compared with the normal group, PWTL decreased significantly (P<0.01) and the expression of p-JNK in the DRG increased in the MPS and MPS-sham-TEAS groups (P<0.01); compared with the MPS group, PWTL was increased significantly (P<0.01) and expression of p-JNK in the DRG was decreased in the MPS+TEAS group. However, when compared with the normal group, PWTL did not recover to baseline and expression of p-JNK was still higher. CONCLUSION: TEAS treatment may produce an analgesic effect, probably by inhibiting the expression of p-JNK in the DRG of rats with MPS.

Dolor miofascial en el territorio craneocervical: Una revisión de la patología y su relación con polimorfismos genéticos del sistema GABAérgico / Myofascial Pain in the craneocervical territory: A review of the pathology and its relationship with the GABAergic system genetic polymorphisms

El dolor miofascial es una patología muscular regional no inflamatoria caracterizada por la presencia de una zona hiperirritable de tejido muscular que se encuentra en una banda tensa, denominado punto gatillo. En la región orofacial pertenece a un conglomerado de patologías denominadas trastornos temporomandibulares, correspondiendo al de mayor prevalencia. Las manifestaciones clínicas van desde dolor local, tensión muscular y disfunción estructural hasta dolor referido, fenómenos autonómicos e hiperexcitabilidad en el sistema nervioso central. Durante las últimas décadas se han asociado variantes genéticas con diferentes expresiones en patologías dolorosas, algunas de las cuales se encuentran en el sistema GABAérgico. En el presente artículo se realiza una revisión del dolor miofascial como patología y su relación con estos polimorfismos genéticos (AU)

Myofascial pain is noninflammatory regional muscular disorder characterized by the presence of a muscle tissue area hyperirritable located on a taut band, called trigger point. In the orofacial region myofascial pain belongs to a cluster of diseases called temporomandibular disorder. Within these pathologies, it is to the most prevalent of its, clinical manifestations include local pain, muscle tension, structural dysfunction, referred pain, autonomic phenomena and hyperexcitability in the central nervous system. During the last decades have been associated genetic variants to painful pathologies, some of which are in the GABAergic system. This article performs a review of myofascial pain as pathology and its relation to genetic polymorphisms in GABAergic system (AU)

Morton's foot and pyridoxal 5'-phosphate deficiency: genetically linked traits.

Vitamin B6 is an essential vitamin needed for many chemical reactions in the human body. It exists as several vitamins forms but pyridoxal 5'-phosphate (PLP) is the phosphorylated form needed for transamination, deamination, and decarboxylation. PLP is important in the production of neurotransmitters, acts as a Schiff base and is essential in the metabolism of homocysteine, a toxic amino acid involved in cardiovascular disease, stroke, thrombotic and Alzheimer's disease. This report announces the connection between a deficit of PLP with a genetically linked physical foot form known as the Morton's foot. Morton's foot has been associated with fibromyalgia/myofascial pain syndrome. Another gene mutation methylenetetrahydrofolate reductase (MTHFr) is now being recognized much commonly than previous with chronic fatigue, chronic Lyme diseases and as "the missing link" in other chronic diseases. PLP deficiency also plays a role in impaired glucose tolerance and may play a much bigger role in the obesity, diabetes, fatty liver and metabolic syndrome. Without the Schiff-base of PLP acting as an electron sink, storing electrons and dispensing them in the mitochondria, free radical damage occurs! The recognition that a phenotypical expression (Morton's foot) of a gene resulting in deficiency of an important cofactor enzyme pyridoxal 5'-phosphate will hopefully alert physicians and nutritionist to these phenomena. Supplementation with PLP, L5-MTHF, B12 and trimethylglycine should be used in those patients with hyperhomocysteinemia and/or MTHFR gene mutation.

Expression of the endocannabinoid system in fibroblasts and myofascial tissues.

The endocannabinoid (eCB) system, like the better-known endorphin system, consists of cell membrane receptors, endogenous ligands and ligand-metabolizing enzymes. Two cannabinoid receptors are known: CB(1) is principally located in the nervous system, whereas CB(2) is primarily associated with the immune system. Two eCB ligands, anandamide (AEA) and 2-arachidonoylglycerol (2-AG), are mimicked by cannabis plant compounds. The first purpose of this paper was to review the eCB system in detail, highlighting aspects of interest to bodyworkers, especially eCB modulation of pain and inflammation. Evidence suggests the eCB system may help resolve myofascial trigger points and relieve symptoms of fibromyalgia. However, expression of the eCB system in myofascial tissues has not been established. The second purpose of this paper was to investigate the eCB system in fibroblasts and other fascia-related cells. The investigation used a bioinformatics approach, obtaining microarray data via the GEO database (www.ncbi.nlm.nih.gov/geo/). GEO data mining revealed that fibroblasts, myofibroblasts, chondrocytes and synoviocytes expressed CB(1), CB(2) and eCB ligand-metabolizing enzymes. Fibroblast CB(1) levels nearly equalled levels expressed by adipocytes. CB(1) levels upregulated after exposure to inflammatory cytokines and equiaxial stretching of fibroblasts. The eCB system affects fibroblast remodeling through lipid rafts associated with focal adhesions and dampens cartilage destruction by decreasing fibroblast-secreted metalloproteinase enzymes. In conclusion, the eCB system helps shape biodynamic embryological development, diminishes nociception and pain, reduces inflammation in myofascial tissues and plays a role in fascial reorganization. Practitioners wield several tools that upregulate eCB activity, including myofascial manipulation, diet and lifestyle modifications, and pharmaceutical approaches.

AlOH3-adjuvanted vaccine-induced macrophagic myofasciitis in rats is influenced by the genetic background.

Macrophagic myofasciitis (MMF) is a specific histopathologic lesion involved in the persistence for years of aluminum hydroxide [Al(OH)(3)] at the site of previous intramuscular (i.m.) injection. In order to study mechanisms involved persistence of MMF lesions, we set up an experimental model of MMF-lesion in Sprague-Dawley and Lewis rat, by i.m. injections of 10 microL of an Al(OH)(3)-adjuvanted vaccine. An evaluation carried out over a 12-month period disclosed significant shrinkage of MMF lesions with time. A radioisotopic study did not show significant aluminium uptake by Al(OH)(3)-loaded macrophages. A morphometric approach showed that Lewis rats with Th1-biased immunity had significantly smaller lesions than Sprague-Dawley rats with balanced Th1/Th2 immunity. Concluding, our results indicate that genetic determinatives of cytotoxic T-cell responses could interfere with the clearance process and condition the persistence of vaccine-induced MMF-lesions.

Clinical study of chronic pain in hereditary myopathies.

In the field of neuromuscular diseases, pain and its management remain imperfectly understood and described. We study 68 unselected, consecutive adult patients attending a multidisciplinary consultation for hereditary myopathy. Forty-six (67%) were suffering from chronic pain. Pain was assessed with self report questionnaire and a standardized clinical evaluation. Mean duration of the pain was 7.2+/-8.9 years, and multiple body sites were involved in 91% of cases. Usual pain intensity (Visual Analogue Scale 0-100) was moderate (39.5+/-26.2). For 42 patients (91%) the principal cause of the pain was of muscular origin, with frequent features of myofascial pain syndromes (MPS, 50%) and fibromyalgia (FMS, 26%). Pain was the major complaint for 6.3% of the patients. Pain management was essentially based on physiotherapy. Only a minority of patients (38%) has an appropriate drug treatment. Common analgesics appeared to be very effective in these patients.