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Tender points/fibromyalgia vs. trigger points/myofascial pain syndrome: a need for clarity in terminology and differential diagnosis.

OBJECTIVE: This study reviews the clinical distinctions between fibromyalgia (FM) and myofascial pain syndrome (MPS), which represent two separate and distinct soft-tissue syndromes. The major aim of this article is to clarify the terminology associated with these syndromes and clearly define the parameters of differential diagnosis and treatment. DATA SOURCES: Pertinent articles in the chiropractic and medical literature are reviewed with an emphasis on the literature published from 1985-1994. STUDY SELECTION: Studies were selected that emphasized differential diagnosis of FM and MPS, as well as individual articles on either FM or MPS. DATA SYNTHESIS: The literature on fibromyalgia and myofascial pain syndromes has grown considerably since 1985. It is now clear that there are several important differences between FM and MPS. The most important criteria for differential diagnosis are the presence of tender points (TePs) and widespread, nonspecific, soft tissue pain in FM, compared with regional and characteristic referred pain patterns with discrete muscular trigger points (TrPs) and taut bands of skeletal muscle in MPS. The etiology of TePs is still unknown and it is uncertain which specific soft tissues are tender in FM patients. Myofascial TrPs are found within a taut band of skeletal muscle and have a characteristic "nodular" texture upon palpation. TrPs are thought to develop after trauma, overuse or prolonged spasm of muscles. Local treatment applied to TePs is ineffective, yet specific treatment of TrPs is often dramatically effective. CONCLUSION: FM and MPS are two different clinical conditions that require different treatment plans. FM is a systemic disease process, apparently caused by dysfunction of the limbic system and/or neuroendocrine axis. It often requires a multidisciplinary treatment approach including psychotherapy, low dose antidepressant medication and a moderate exercise program. MPS is a condition that arises from the referred pain and muscle dysfunction caused by TrPs, which often respond to manual treatment methods such as ischemic compression and various specific stretching techniques. Both of these conditions are seen routinely in chiropractic offices; therefore, it is important for field practitioners to understand these distinctions.

Chiropractic↗

[Dynamic cardiomyoplasty].

Between 1965 and 1995 the incidence of heart failure has been constantly rising and the mortality from this disease has increased fivefold. The introduction of ACE-inhibitors and of adrenergic beta-blockers have resulted in major symptomatic improvements in patients with mild to moderate heart failure. For end-stage disease, heart transplantation offers by now the only therapeutic option and yields excellent results. The permanent implantation of left heart assist-devices is just gaining increasing importance. Yet, both methods also have inherent drawbacks and may not be available to all patients, so that new methods are constantly evaluated. Cardiomyoplasty was introduced into clinical practice in 1985 by Alain Carpentier and since then more than 700 patients have been operated worldwide. After dissection of the latissimus dorsi muscle it is wrapped around the heart in a clockwise fashion (Figure 1). Two sensing electrodes are placed on the anterior aspect of the right ventricle and two stimulation electrodes between the proximal branches of the thoracodorsal nerve (Medtronic SP 5548). The electrodes are then connected with a burststimulator (Cardiomyostimulator, Medtronic 4710) (Figure 2). During the first 2 weeks following the operation the muscle is not stimulated in order to allow for the healing process. Thereafter, a stimulation protocol with a programmed, staged increase of the stimulation frequency is started, to induce transformation of the skeletal muscle into a "fatigue resistant" tissue. After 3 months the muscle is stimulated with every second heart beat (2:1 mode) with full burstimpulses containing 6 single impulses per burst for a duration of 185 ms (Figure 3). Cardiomyoplasty was conceived for patients in NYHA III and severely impaired myocardial function, in whom drug treatment does not produce the expected benefits. The criteria for patient selection are strictly followed, since it has been shown in the past, that the preoperative condition of the patient is of specific importance for the postoperative outcome. Contraindications are NYHA IV, advanced right ventricular dysfunction, secondary pulmonary hypertension (> 600 dyn x s x cm-5), LV end-diastolic diameter > 70 mm und AV-valve incompetence > Grad II. Between July 1985 und October 1996 647 patients received a cardiomyoplasty with the Medtronic Cardiomyoplasty System and the results from 438 patients were analyzed from the "Worldwide Cardiomyoplasty Study Group". One and 2 years following the operation NYHA-class had improved by one class in 41.9% and 53.3%, respectively, and by 2 classes in 38.1% and 30.5%, respectively. In 16% and 15% no improvement was found (Figure 4). Prospective investigation of the quality of life by a score revealed a considerable improvement in the level of daily activities and social interaction. In contrast, two years after the operation, only a small, but significant increase in LV-EF from 22.9 +/- 8.1% to 25.8 +/- 9.7% (p < 0.05) was shown. Heart rate, maximal O2-consumption, total exercise time, cardiac index, stroke volume and stroke work index did not change. According to the results of a recent FDA-study, in-hospital mortality was 12% between 1991 and 1993, and was reduced during a second phase starting 1994 to < 3%. One, 2 and 3-year survival of 349 patients who were in NYHA-III prior to the operation was 69%, 56% und 47%, respectively. 43 patients who were operated in NYHA IV exhibited considerably worse survival with only 48% after 1 year and 30% after 2 years, respectively. In a subgroup of 103 patients with a statistically low operative risk, 1, 2 and 3-year survival was 77%, 71% und 61%, respectively (Figure 5). As a mechanism of action the skeletal muscle wrap exerts some active improvement of systolic wall motion of the heart/skeletal muscle complex. However, probably more important is an acute and chronically persisting shift of the pressure-volume relation to the left. This process results in a "reverse remodel

Cardiomyoplasty↗

Effects of chronic heart failure on skeletal muscle vascular transport capacity of rats.

The purpose of this study was to determine the effects of chronic heart failure (HF) on the vascular transport capacity of rat skeletal muscle. A large myocardial infarction (MI) was surgically produced in rats by ligating the left main coronary artery (n = 10). Sham operations were performed in control animals (Sham, n = 4). The vascular transport capacity of each animal's hindquarters was determined 8-9 mo post-MI to ensure that each rat was in a chronic state of left ventricular (LV) dysfunction and HF. With the use of an isolated, maximally vasodilated hindquarters preparation, we found that perfusion pressures, capillary pressures, capillary filtration coefficients, and precapillary vascular resistances were similar for the two groups under isogravimetric conditions. In contrast, postcapillary resistance was elevated (Sham, 0.9 +/- 0.2; MI, 1.5 +/- 0.2 mmHg.ml-1 x min x 100 g; P = 0.03), and flow to the hindquarters was reduced for rats in chronic HF compared with controls (Sham, 16.1 +/- 2.3; MI, 12.1 +/- 0.9 ml.min-1 x 100 g-1; P = 0.07). Vascular flow capacity (VFC) for the hindquarters was similar for control rats and rats with chronic HF across a wide range of perfusion pressures (20-60 mmHg). However, regional flow capacities were reduced in soleus and red gastrocnemius but not in white gastrocnemius muscles of rats in chronic HF compared with controls. These results suggest that the VFC of muscle comprised primarily of high oxidative fibers is selectively reduced in rats with chronic HF.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Serum enzymes in hypothyroidism.

AIM: To report three cases of hypothyroidism detected because of unexplained elevation of serum enzyme levels on biochemical testing. METHODS: Clinical details and serum enzyme results were obtained before and after L-thyroxine (T4) replacement therapy. RESULTS: The three patients all had serum creatine kinase (CK) levels > 2000 U/L, aspartate aminotransferase (AST) > 90 U/L, and lactate dehydrogenase (LD) > 300 U/L at presentation, with these levels being 10-15, 2-6, and 2-3 times the upper reference limits respectively. CK isoenzyme determination was consistent with skeletal muscle origin. Thyroid function tests performed after consultation with the clinical biochemist confirmed the biochemical diagnosis of primary hypothyroidism. A rapid fall toward normal serum enzyme levels occurred in response to T4 replacement therapy. CONCLUSIONS: Although serum enzymes are an integral part of both the liver and cardiac profiles provided by laboratory, they are not organ specific, and changes may reflect dysfunction elsewhere in the body. Elevations of serum CK (and other muscle enzymes) may occur in hypothyroid subjects, the cause of which has not been established. The clinical diagnosis of hypothyroidism requires a high index of suspicion and should be considered in patients with unexplained persistent elevations of serum muscle enzymes.

Adult↗

Molecular interaction between nitric oxide and ryanodine receptors of skeletal and cardiac sarcoplasmic reticulum.

In striated muscle, the sarcoplasmic reticulum (SR) is the major storage compartment of intracellular Ca2+ that controls cytosolic free Ca2+ (Cai) and developed force by sequestering and releasing Ca2+ during each contraction. Ca2+ release from the SR occurs through high-conductance Ca2+ release channels or ryanodine receptors (RyR), which are regulated by various signaling processes. Over the last 15 years, there has been a growing consensus that critical sulfhydryl sites on RyRs can be oxidized and reduced, respectively, to open and close the release channels. The pharmacological actions of various classes of sulfhydryl reagents have demonstrated the existence of hyperreactive thiols on RyRs, which could play a role in the regulation of normal contractile function and explain contractile dysfunctions in pathological conditions. More recent studies show that redox regulation of release channels may occur by nitric oxide (NO), a physiological signaling mechanism. This article is intended to review current concepts in thiol regulation of RyRs and present new data on the possible identification of the primary cysteine residues, which may be the site of oxidation and S-nitrosylation involved in channel opening.

Animals↗

Lower leg muscle atrophy in ankle osteoarthritis.

The aim of this study was to determine changes in the lower leg muscles associated with ankle osteoarthritis. Fifteen unilateral ankle osteoarthritis patients and fifteen age-gender-matched normal subjects were assessed with clinical [osteoarthritis latency time, pain, alignment, AOFAS ankle score, ankle range of motion (ROM), calf circumference], radiological (ankle osteoarthritis grading), and muscular-physiological parameters [isometric maximal voluntary ankle torque, surface electromyography of the anterior tibial (AT), medial gastrocnemius (MG), soleus (SO), and peroneus longus (PL) muscle]. The osteoarthritis patients had increased pain (6.8 points) and reduced AOFAS score (33.7 points) compared to the control group. Compared to the contralateral healthy leg, the arthritic leg showed reduced mean dorsi-/plantar flexion ROM (16.0 degrees), reduced mean calf circumference (2.1 cm), smaller mean dorsiflexion (16.4 Nm) and plantar flexion (15.8 Nm) torques, lower mean electromyography frequency for all muscles (AT -22.6 Hz; MG -27.3 Hz; SO -25.9 Hz; PL -28.5 Hz), and lower mean electromyography intensity in the AT [-28.0x10(3) (microv)2], MG [-13.3x10(3) (microv)2], and PL [-12.8x10(3) (microv)2]. SO mean electromyography intensity was not significantly changed [+2.0x10(3) (microv)2]. Unilateral ankle osteoarthritis is associated with atrophic changes of the lower leg muscles. This study supports previous observations on muscle dysfunction in knee osteoarthritis.

Adult↗

Pelvic floor electromyography in men with chronic pelvic pain syndrome: a case-control study.

AIMS: The objectives of this study were (1) to identify differences between men with chronic pelvic pain syndrome (CPPS), compared with pain-free men, in surface electromyography/biofeedback (sEMG/BFB) readings of pelvic floor muscles and (2) to determine which pelvic floor muscle sEMG readings may have differential diagnostic and treatment selection value by accurately predicting group membership, CPPS versus normal. METHODS: Twenty-one men with CPPS and 21 healthy men without pelvic pain underwent a standardized sEMG examination by a licensed physical therapist. RESULTS: On group difference measures men with CPPS showed significantly greater sEMG instability in preliminary resting baseline. Three sEMG measures reliably categorized CPPS versus normals with CPPS showing greater preliminary resting baseline hypertonicity and instability with lowered voluntary endurance contraction amplitude. CONCLUSIONS: CPPS patients manifest pelvic floor muscle instability compared to normals. Prebaseline resting hypertonicity and instability along with endurance contraction weakness reliably predicts subject membership in the CPPS vs. normal group. Pelvic floor muscle sEMG may be a valuable screening tool to identify patients with CPPS who may benefit from therapies aimed at correcting pelvic floor muscle dysfunction.

Adolescent↗

Design of a torque-controlled manipulator to analyse the admittance of the wrist joint.

This paper describes the design of a torque-controlled manipulator to identify the dynamics of the wrist joint. With torque disturbances, the subject can actively control the joint angle, giving a natural task. The application of a hybrid haptic controller guarantees linearity over a large bandwidth and adjustable virtual dynamics. The haptic controller has a bandwidth of 50 Hz, meaning that the virtual dynamics are realistically felt at up to 50 Hz. To let the subject 'feel' the torque, disturbances as well as possible the apparent, or virtual, dynamics of the device must be small. The minimal apparent inertia of the device is 1.6 g m(2), which is of the same order as for a normal wrist, and the minimal damping and stiffness are negligible. To judge the accuracy of the manipulator, loads of known physical properties were attached and their parameters were quantified. The parameters of the loads were estimated with a maximum error of 5%. As the eigenfrequency of a (co)-contracted human wrist is approximately 15 Hz, the 50-Hz bandwidth of the haptic device is sufficient to measure all relevant dynamics of the human wrist. With this device, the dynamics of the human wrist joint can be measured under varying virtual dynamics, as well as the effect of neurological dysfunction on human motor control, for example.

Algorithms↗

Propagation disturbance of motor unit action potentials during transient paresis in generalized myotonia: a high-density surface EMG study.

Patients with autosomal recessive generalized myotonia, or Becker's disease, often suffer from a peculiar transient paresis. As yet, the relationship between this transient paresis and the defect in the gene encoding for a voltage gated Cl- channel protein in the muscle membrane of these patients is unclear. In order to gain a better understanding of the electrophysiological properties of the muscle fibre membrane in these generalized myotonia patients, we have studied transient paresis with a novel high-density surface EMG (sEMG) technique. We conclude that the transient paresis is explained by a deteriorating muscle membrane function, ending in conduction block and paresis. Multi-channel sEMG during the period of force decline in transient paresis shows a decrease in peak-peak amplitude of the motor unit action potentials from endplate towards tendon. This disturbance increases with time and place, indicating a deteriorating membrane function, and ends in a complete blocking of propagation within seconds. Spatiotemporally, this leads to a V-shaped sEMG pattern. In a more general sense, this contribution shows how spatiotemporal information, available through non-invasive high-density sEMG, may provide novel insights into electrophysiological aspects of membrane dysfunction.

Action Potentials↗

Quantification of cocontraction in spastic cerebral palsy.

Antagonist cocontraction was hypothesized to limit net moment production in children with spastic diplegic cerebral palsy (CP). A second hypothesis was that concontraction would vary with joint angle. To test these hypotheses, surface EMG activity and moment data from the quadriceps and hamstrings muscle groups were obtained from children with CP and compared with normally developing children during isometric flexion and extension exertions. A biomechanical model was developed to predict individual moments produced by the agonist and antagonist muscle groups. Concontraction was defined as the percentage of the net moment that was negated by the antagonist moment. The model performed well in predicting the measured moment as illustrated by high R2 correlation coefficients and low prediction errors. The mean maximum moment produced was greater in normally developing children than children with CP in both flexion and extension. Antagonist cocontraction during extension was greater in children with CP (12.2 +/- 14.4%) than in normally developing children (4.9 +/- 3.8%), implying that antagonist cocontraction is one explanation for the observed extension weakness in children with CP. However, during flexion, cocontraction was not significantly different between the two groups. Cocontraction differed significantly with joint angle in both groups during flexion and in the normally developing children during extension. Although quantifying coactivation based on EMG activity alone produced similar results, it underestimated the effect of the antagonist. The quantification of cocontraction has potential applications for characterizing spastic muscle dysfunction and thereby improving clinical outcomes in children with CP.

Adolescent↗

Contraction of the pelvic floor muscles during abdominal maneuvers.

OBJECTIVE: To determine whether voluntary abdominal muscle contraction is associated with pelvic floor muscle activity. DESIGN: Pelvic floor muscle activity was recorded during contractions of the abdominal muscles at 3 different intensities in supine and standing positions. SETTING: Research laboratory. PARTICIPANTS: Six women and 1 man with no histories of lower back pain. INTERVENTION: Not applicable. MAIN OUTCOME MEASURES: Electromyographic activity of the pelvic floor muscles was recorded with surface electrodes inserted into the anus and vagina. These recordings were corroborated by measurements of anal and vaginal pressures. Gastric pressure was recorded in 2 subjects. RESULTS: Pelvic floor muscle electromyography increased with contraction of the abdominal muscles. With strong abdominal contraction, pelvic floor muscle activity did not differ from that recorded during a maximal pelvic floor muscle effort. The pressure recordings confirmed these data. The increase in pressure recorded in the anus and vagina preceded the pressure in the abdomen. CONCLUSIONS: In healthy subjects, voluntary activity in the abdominal muscles results in increased pelvic floor muscle activity. The increase in pelvic floor pressure before the increase in the abdomen pressure indicates that this response is preprogrammed. Dysfunction of the pelvic floor muscles can result in urinary and fecal incontinence. Abdominal muscle training to rehabilitate those muscles may be useful in treating these conditions.

Abdominal Muscles↗

The impact of self-retaining retractors on the paraspinal muscles during posterior spinal surgery.

STUDY DESIGN: This was a prospective pilot study examining pre-, intra- and postoperative measures. OBJECTIVES: The aim of the study was to investigate the effect of muscle retractors on the posterior spinal muscles during posterior spinal surgery. SUMMARY OF BACKGROUND DATA: Previous studies have identified changes in the structure and function of the back extensor mechanism as a result of low back pain. However, the effect of surgery on the functioning of these muscles, particularly surgical retraction, has received less attention. METHODS: Twenty patients undergoing posterior spinal surgery were recruited into this study, and recordings of intramuscular pressure during surgery were performed using a pressure-monitoring system before insertion of retractors, 5, 30, and 60 minutes into surgery, and on removal of retractors. Before and following use of the retractors, muscle biopsies were taken from the multifidus muscle for analysis using birefringence techniques. RESULTS: A significant increase in intramuscular pressure (P < 0.001) was observed during surgery. On removal of retractors, this pressure returned to or near to the original value. Analysis of muscle biopsies using calcium activated adenosine triphosphatase birefringence revealed a reduction in muscle function following prolonged use of self-retaining retractors. CONCLUSIONS: A substantial rise in pressure in the erector spinae muscle during posterior spinal surgery was observed, and this appeared to be associated with marked changes in the function of the muscles. This could be an important factor in the generation of operative scar tissue and postoperative dysfunction of the spinal muscles.

Adult↗

Bilateral gait patterns in subjects fitted with a total hip prosthesis.

OBJECTIVES: The purpose of this report was to determine whether the muscle powers and the mechanical energies developed during the push-off period of the gait cycle of patients having a total hip prosthesis were different from able-bodied subjects as well as the effect on the nonoperated limb. DESIGN: Case control study. SETTING: All patients where independent and functional. PATIENTS: Four patients participated in the study. The indication for surgery was degenerative arthritis of the hip. There was also an able-bodied group. INTERVENTION: A Harris-Galante total hip prosthesis was used to restore hip stability and function. The patients were all operated on by the same orthopedic surgeon and had the same type of total hip replacement. MAIN OUTCOME MEASURE: Gait analyses showed that not only the hips of the surgical group were affected but also the knees. RESULTS: Peak power did not show any significant difference except for a decrease in the frontal plane of the operated hip power absorption. The operated hip developed 35% and 48% less energy than that of the able-bodied group in the sagittal and frontal planes, respectively. The nonoperated hip was also affected and developed 35% more energy in the sagittal plane than the operated limb but 20% less than that of the able-bodied group. There was a reduction of 47% in the energies developed in the knees of the surgical patient group. CONCLUSION: These results confirmed the presence of some mechanical dysfunction in the nonoperated limb.

Aged↗

Cutaneous reflexes in patients with acute lacunar infarctions.

Cutaneous reflex (CR) was measured in 15 patients with acute lacunar stroke and in 15 age- and sex-matched normal subjects. EMG activities were recorded from the first dorsal interosseous muscle with surface electrodes, rectified and averaged. Intensity of the stimulation on the index finger was four times the sensory threshold. Aided by audio- and visual-feedback monitoring, the subjects abducted the index finger. Side-to-side comparison was made on all the subjects. CR abnormalities were found in all of our patients. The early inhibitory (I1) and second excitatory (E2) components were attenuated in 11 of 15 patients. The I1-E2 interpeak amplitude (A2) was significantly reduced in all the patients. Prolonged latency of I1-E2 components was found to be pronounced in six of eight patients with sensory symptoms. Eight patients were followed up 1 month later. By that time, the abnormal CR had reversed to some degree in all of them. CR alternation was still present in two fully recovered patients. Our results implied a thalamic relay in the afferent limb of the CR. CR could be a valuable adjunct for assessing long tract dysfunction and monitoring functional recovery.

Aged↗

Structural and biochemical evidence of mitochondrial depletion in pigs with hypertrophic cardiomyopathy.

Pig hearts with naturally occurring hypertrophic cardiomyopathy (HCM) were isolated to investigate the effects of mitochondrial deficiency at biochemical and molecular levels. Enzyme activities of mitochondrial-encoded cytochrome c oxidase and NADH dehydrogenase in the HCM hearts (n=12) were lower than that in the controls (n=12) by 41+/-29% (P<0.01) and 43+/-21% (P<0.001), respectively. Additionally, Southern blot analysis was conducted to quantify the relative amount of mitochondrial DNA (mtDNA) from the HCM and controls. The relative amount of mtDNA in the HCM hearts was significantly 57+/-19% (P<0.001) lower than that in the controls. Both mitochondrial enzyme deficiency and mtDNA depletion were significantly correlated with the degree of cardiac hypertrophy judged based on the ratio of heart/body weight. In conclusion, our results reveal that a secondary effect of tissue-specific mtDNA depletion and mitochondrial dysfunction is in response to the HCM.

Animals↗

Mitochondrial DNA deletion mutations: a causal role in sarcopenia.

Mitochondrial DNA (mtDNA) deletion mutations accumulate with age in tissues of a variety of species. Although the relatively low calculated abundance of these deletion mutations in whole tissue homogenates led some investigators to suggest that these mutations do not have any physiological impact, their focal and segmental accumulation suggests that they can, and do, accumulate to levels sufficient to affect the metabolism of a tissue. This phenomenon is most clearly demonstrated in skeletal muscle, where the accumulation of mtDNA deletion mutations remove critical subunits that encode for the electron transport system (ETS). In this review, we detail and provide evidence for a molecular basis of muscle fiber loss with age. Our data suggest that the mtDNA deletion mutations, which are generated in tissues with age, cause muscle fiber loss. Within a fiber, the process begins with a mtDNA replication error, an error that results in a loss of 25-80% of the mitochondrial genome. This smaller genome is replicated and, through a process not well understood, eventually comprises the majority of mtDNA within the small affected region of the muscle fiber. The preponderance of the smaller genomes results in a dysfunctional ETS in the affected area. As a consequence of both the decline in energy production and the increase in oxidative damage in the region, the fiber is no longer capable of self-maintenance, resulting in the observed intrafiber atrophy and fiber breakage. We are therefore proposing that a process contained within a very small region of a muscle fiber can result in breakage and loss of muscle fiber from the tissue.

Aging↗

Effects of ascorbic acid on lead induced alterations of synaptic transmission and contractile features in murine dorsiflexor muscle.

Lead is a common environmental toxin that affects neuromuscular junction and potentially might cause muscle weakness. Antioxidants like ascorbic acid may protect against lead induced myopathy. The present study measured isometric twitch tensions (evoked either directly by muscle stimulation or indirectly by nerve stimulation) to study effects of ascorbic acid on lead induced alterations at murine dorsiflexor skeletal muscle. Resting membrane potentials (RMPs), endplate potentials (EPPs) and miniature endplate potentials (MEPPs) were also recorded. Forty animals were divided into four groups of n = 10 each. (10 control, 10 lead alone, 10 ascorbic acid alone, 10 lead treated plus ascorbic acid). Lead (1 mg/kg) i.p, was administered daily for 2 weeks before the recording day and ascorbic acid (200 mg/kg, i.p) was given daily for 3 weeks prior to the experiment day. Lead treatment reduced twitch tension significantly (from 4.3 +/- 0.5 g to 2.7 +/- 0.2 g) and delayed half time of decay compared to the control. Similarly MEPPs frequencies were reduced following lead treatment. Application of ascorbic acid prevented twitch tension reduction in lead treated mice (3.3 +/- 0.3 g) and reversed lead induced delay in half time of decay. The negative actions of lead treatment on MEPPs frequencies were also modified with ascorbic acid. It appears that ascorbic acid exerts a protective role against lead induced peripheral nerve and muscle dysfunction. This effect of ascorbic acid on lead induced neuromyopathy is probably mediated via a free radical scavenging mechanism or modification of Ca(2+) homeostasis.

Animals↗