EMG biofeedback with upper extremity musculature for relaxation training: a critical review of the literature

A critical review is presented of studies utilizing EMG biofeedback for relaxation of upper extremity musculature. Examined are experimental investigations with normal subjects and those with psychological problems, and clinical applications of the methodology for treatment of involuntary movements and anxiety. Articles are reviewed in terms of procedures, controls and results. It is determined that few valid conclusions can be drawn regarding the efficacy of upper extremity EMG biofeedback for relaxation and that further research is required prior to utilizing the technique clinically. Suggestions are offered for areas of investigation.     

EMG biofeedback for handwriting disabilities: a critical examination of the literature

A critical examination of the literature on the use of electromyographic (EMG) biofeedback for problems of handwriting is presented. Examined are the procedures, results and conclusions of clinical treatments of writer's cramp and the habilitation of writing. The major flaws in each study are discussed and conclusions drawn from the review are presented, the primary one being that EMG biofeedback of the muscles of the upper extremity has yet to be demonstrated as a treatment of choice for handwriting disabilities. The lack of a sound foundation of data is seen as the main reason for the paucity of investigations in this particular area. Suggestions for further work are offered.     

Serotonin,glutamate and glycerol are released after the injection of hypertonic saline into human masseter muscles – a microdialysis study

Background

Chronic myalgia is associated with higher muscle levels of certain algesic biomarkers. The aim of this study was to investigate if hypertonic saline-induced jaw myalgia also leads to release of such biomarkers and if there were any sex differences in this respect.

Methods

Healthy participants, 15 men and 15 aged-matched women (25.7 ± 4.3 years) participated. Intramuscular microdialysis into masseter muscles was performed to sample serotonin (5-HT), glutamate, lactate, pyruvate, glucose and glycerol. After 2 hours 0.2 mL hypertonic saline (58.5 mg/mL) was injected into the masseter on one side and 0.2 mL isotonic saline (9 mg/mL) into the contralateral masseter close to the microdialysis catheter. Microdialysis continued for 1 hour after the injections. Pressure pain thresholds (PPT) and pain were assessed before and after injections.

Results

The median (IQR) peak pain intensity (0–100 visual analogue scale) after hypertonic saline was 52.5 (38.0) and after isotonic saline 7.5 (24.0) (p < 0.05). 5-HT, glutamate and glycerol increased after hypertonic saline injection (p < 0.05). Lactate, pyruvate and glucose showed no change. PPT after microdialysis was reduced on both sides (p < 0.05) but without side differences. Pain after hypertonic saline injection correlated positively to 5-HT (p < 0.05) and negatively to glycerol (p < 0.05).

Conclusions

5-HT, glutamate and glycerol increased after a painful hypertonic saline injection into the masseter muscle, but without sex differences. Since increased levels of 5-HT and glutamate have been reported in chronic myalgia, this strengthens the validity of the pain model. Glycerol warrants further investigations.     

Expression of 5-HT3 receptors and TTX resistant sodium channels (NaV1.8) on muscle nerve fibers in pain-free humans and patients with chronic myofascial temporomandibular disorders

Background

Previous studies have shown that 5-HT₃-antagonists reduce muscle pain, but there are no studies that have investigated the expression of 5-HT₃-receptors in human muscles. Also, tetrodotoxin resistant voltage gated sodium-channels (Na_V) are involved in peripheral sensitization and found in trigeminal ganglion neurons innervating the rat masseter muscle. This study aimed to investigate the frequency of nerve fibers that express 5-HT_3A-receptors alone and in combination with Na_V1.8 sodium-channels in human muscles and to compare it between healthy pain-free men and women, the pain-free masseter and tibialis anterior muscles, and patients with myofascial temporomandibular disorders (TMD) and pain-free controls.

Methods

Three microbiopsies were obtained from the most bulky part of the tibialis and masseter muscles of seven and six healthy men and seven and six age-matched healthy women, respectively, while traditional open biopsies were obtained from the most painful spot of the masseter of five female patients and from a similar region of the masseter muscle of five healthy, age-matched women. The biopsies were processed by routine immunohistochemical methods. The biopsy sections were incubated with monoclonal antibodies against the specific axonal marker PGP 9.5, and polyclonal antibodies against the 5-HT_3A-receptors and Na_V1.8 sodium-channels.

Results

A similar percentage of nerve fibers in the healthy masseter (85.2%) and tibialis (88.7%) muscles expressed 5-HT_3A-receptors. The expression of Na_V1.8 by 5-HT_3A positive nerve fibers associated with connective tissue was significantly higher than nerve fibers associated with myocytes (P < .001). In the patients, significantly more fibers per section were found with an average of 3.8 ± 3 fibers per section in the masseter muscle compared to 2.7 ± 0.2 in the healthy controls (P = .024). Further, the frequency of nerve fibers that co-expressed Na_V1.8 and 5-HT_3A receptors was significantly higher in patients (42.6%) compared to healthy controls (12.0%) (P < .001).

Conclusions

This study showed that the 5-HT_3A-receptor is highly expressed in human masseter and tibialis muscles and that there are more nerve fibers that express 5-HT_3A-receptors in the masseter of women with myofascial TMD compared to healthy women. These findings indicate that 5-HT₃-receptors might be up-regulated in myofascial TMD and could serve as potential biomarkers of chronic muscle pain.     

The effect of apolipoprotein E polymorphism on the response to lipid-lowering treatment with atorvastatin or fenofibrate

Although the effect of apolipoprotein E gene polymorphism on the response to treatment with statins has been studied, the results are conflicting. Moreover, little is known about the possible effect of apolipoprotein E alleles on the response to treatment with fibrates. The purpose of this study was to evaluate the effect of apolipoprotein E polymorphism on lipid-lowering response to treatment with atorvastatin and fenofibrate in patients with different types of dyslipidemia. The study population included 136 patients with heterozygous familial hypercholesterolemia (type IIA dyslipidemia) treated with atorvastatin (20 mg/day) and 136 patients with either primary hypertriglyceridemia (type IV dyslipidemia) or mixed hyperlipidemia (type IIB dyslipidemia) treated with micronized fenofibrate (200 mg/day). Overall, no significant associations were detected between apolipoprotein E genotype and response to treatment with atorvastatin. In patients treated with fenofibrate, significant associations were noted between apolipoprotein E genotype and changes in apolipoprotein B, apolipoprotein E and triglyceride levels. Specifically, in apolipoprotein E2, apolipoprotein E3, and apolipoprotein E4 individuals, apolipoprotein B reductions were 22%, 17%, and 8%, respectively (P = .003); apolipoprotein E reductions were 45%, 20%, and 15%, respectively (P = .006); whereas triglyceride reductions reached 53%, 36%, and 33%, respectively (P = .033). In conclusion, apolipoprotein E genotype had no significant effect on the response to treatment with atorvastatin in patients with heterozygous familial hypercholesterolemia, but in patients with primary hypertriglyceridemia or mixed hyperlipidemia, there was a clear association between apolipoprotein E genotype and response to treatment with fenofibrate.     

A cross-modality approach for treatment of chronic pain: a preliminary report

Three subjects, presenting a variety of chronic pain problems, were treated with a cross-modality feedback technique. Their presenting pain intensity was matched to a pure tone auditory stimulus decibel level and in each session this stimulus was progressively reduced in loudness, with the subjects having the task of reducing their pain to match each new, lower decibel levels. Audiometric measures, responses to pain assessment scales, self-reports, reports from hospital staff, and reductions in pain medications all demonstrated marked pain reduction in all cases. Follow-up assessments revealed that the improvements were maintained long after treatment had been discontinued.