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PubMed2005

[Two children with skin rash and muscle weakness: juvenile dermatomyositis].

Two girls aged 1.5 and 3 years, presented with a skin rash, loss of proximal muscle power and malaise. The younger girl recovered quickly after a short course of corticosteroids but the elder girl proved more difficult to treat effectively with corticosteroids, methotrexate, ciclosporin, intravenous immunoglobulins and hydroxychloroquine. This combination of symptoms should make one consider the diagnosis of juvenile dermatomyositis (JDM). To make the diagnosis of JDM, a characteristic skin rash, proximal muscle weakness, elevated muscle enzymes and, possibly, an abnormal EMG or muscle biopsy should be present. Treatment consists, of steroids and, if necessary, immunosuppressive agents or intravenous immunoglobulins. If cutaneous lesions are serious or persistent, hydroxychloroquine may also be prescribed.

Anti-Inflammatory Agents↗

PubMed1989

Increased muscular fatigue in patients with neurogenic muscle weakness: quantification and pathophysiology.

The strength of maximum voluntary contraction (MVC) and muscular fatigue measured from ankle dorsiflexors and knee extensors of 15 patients with neurogenic muscle weakness was compared with those of 20 healthy subjects. Muscle weakness, defined as the failure to generate the expected force, was determined by two methods: (1) manual muscle testing and (2) measurement of MVC using a force transducer. Muscle strength was then quantified as the MVC in Newtons (N)/kg body weight. The percent decrease in both MVC (the Fatigue Index [FI]), and rectified-integrated electromyogram (RIEMG) at the end of 60sec of sustained MVC were computed. There were three main findings. (1) Muscle strength was significantly (p less than 0.001) reduced in both muscles of the patient group: in ankle dorsiflexors, means = 1.62 +/- 0.7N/kg vs 4.8 +/- 0.5N/kg; in knee extensors, means = 3.2 +/- 1.8N/kg vs 7.8 +/- 1.5N/kg. (2) Fatigue was significantly greater (p less than 0.01) in the patient group: for ankle dorsiflexors, means = 50 +/- 15% vs 34 +/- 13%; and for knee extensors, means = 62 +/- 17% vs 46 +/- 15%. There was a negative correlation between muscle strength and FI of only the knee extensors of the patients (r = -0.88, p less than 0.001). (3) The mean decline in RIEMG of the two muscles combined was also significantly greater (p less than 0.001) in the patient group (means = 48 +/- 16% vs 2 +/- 11%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1994

Adult Fanconi syndrome with proximal muscle weakness and hypophosphatemic osteomalacia: report of a case.

A 42-year-old female presented with progressive proximal muscle weakness, generalized hyperreflexia, marked bone pain, severe lumbago and knee arthralgia. Electromyographic study showed short-duration (5-10 msec), variable amplitude (200-2500 microV) polyphasic potentials. A muscle biopsy specimen revealed non-specific type II fiber atrophy. After a comprehensive laboratory work-up, adult Fanconi syndrome was diagnosed. The patient's symptoms, including bone pain and proximal muscle weakness, were relieved after a six-week supplement of tricalcium phosphate, vitamin D3 and sodium bicarbonate. The hyperreflexia also became less brisk.

Adult↗

PubMed2002

Muscle weakness and cocontraction in upper limb hemiparesis: relationship to motor impairment and physical disability.

The purpose of this article is to describe the relationship between poststroke upper limb muscle weakness and cocontraction, and clinical measures of upper limb motor impairment and physical disability. Electrormyographic (EMG) activity of the paretic and nonparetic wrist flexors and extensors of 26 chronic stroke survivors were recorded during isometric wrist flexion and extension. The root mean square (RMS) of the EMG signal was used as a measure of strength of contraction. A ratio of RMS of antagonist and agonist muscles was used as a measure of cocontraction. Upper limb motor impairment and physical disability were assessed with the Fugl-Meyer motor assessment (FMA) and the arm motor ability test (AMAT), respectively. The strength of muscle contraction was significantly stronger in the nonparetic limb (P < 0.001). The degree of cocontraction was significantly greater in the paretic limb (P < 0.001). The strength of muscle contraction in the paretic limb correlated significantly with FMA (r = 0.62 to 0.87, P < or = 0.001) and AMAT (r = 0.66 to 0.80, P < or = 0.001) scores. Similarly, the degree of cocontraction correlated significantly with FMA (r = -0. 70 to -0.64, P < or = 0.001) and AMAT (r = -0. 72 to -0.62, P < or = 0.001) scores. Muscle weakness and degree of cocontraction correlate significantly with motor impairment and physical disability in upper limb hemiplegia. This relationship may provide insights toward development of specific interventions. However, additional studies are needed to demonstrate a cause and effect relationship.

Adult↗

PubMed1984

Reversible hypercapnic respiratory insufficiency in scleroderma caused by respiratory muscle weakness.

A patient with scleroderma presented with hypercapnic respiratory failure. Evaluation of pulmonary mechanics revealed severe restriction caused in part by respiratory muscle weakness. Treatment with prednisone corrected hypoventilation, improved symptoms, increased lung volumes, returned respiratory muscle strength to normal range, but did not change the degree of lung stiffness. This case demonstrates that restrictive patterns in scleroderma can be due to either lung or chest wall disease and that the latter may be reversible. If respiratory muscle weakness is present with restrictive ventilatory patterns in patients with scleroderma, a therapeutic trial of corticosteroid is warranted.

Humans↗

PubMed1992

Inspiratory muscle weakness and dyspnea in chronic heart failure.

Dyspnea is a common, disabling symptom in chronic heart failure, yet the underlying mechanisms remain unknown. The respiratory muscle pump is composed of skeletal muscles whose strength directly influences the pump's performance. Respiratory muscle weakness is important in the dyspnea experienced by some patients with pulmonary disease; however, the role of the respiratory muscle pump in the dyspnea of chronic heart failure has not previously been examined. To assess respiratory muscle strength and its relation to dyspnea during daily activity, we measured maximum inspiratory and expiratory mouth pressures as indices of respiratory muscle strength and the baseline dyspnea index in nine stable, chronic cardiac pump failure patients who had no evidence of primary lung disease, and in nine age- and sex-matched healthy control subjects. The chronic heart failure patients, when compared with their matched control subjects, had reduced inspiratory and expiratory muscle strength, and both inspiratory and expiratory muscle strength were significantly correlated with dyspnea during daily activity (r2 = 0.80, p = 0.001 and r2 = 0.45, p = 0.05, respectively). Inspiratory muscle strength accounted for all of the variance in dyspnea that was correlated with respiratory muscle strength when the relative contributions of inspiratory and expiratory muscle strength were examined. There was no correlation between lung volumes or spirometry and dyspnea in the heart failure patients. These findings indicate that patients with stable chronic heart failure have inspiratory and expiratory muscle weakness and further suggest that the respiratory muscle pump significantly contributes to the dyspnea during the activities of daily living.

Activities of Daily Living↗

PubMed2002

Zmpste24 deficiency in mice causes spontaneous bone fractures, muscle weakness, and a prelamin A processing defect.

Zmpste24 is an integral membrane metalloproteinase of the endoplasmic reticulum. Biochemical studies of tissues from Zmpste24-deficient mice (Zmpste24(-/-)) have indicated a role for Zmpste24 in the processing of CAAX-type prenylated proteins. Here, we report the pathologic consequences of Zmpste24 deficiency in mice. Zmpste24(-/-) mice gain weight slowly, appear malnourished, and exhibit progressive hair loss. The most striking pathologic phenotype is multiple spontaneous bone fractures-akin to those occurring in mouse models of osteogenesis imperfecta. Cortical and trabecular bone volumes are significantly reduced in Zmpste24(-/-) mice. Zmpste24(-/-) mice also manifested muscle weakness in the lower and upper extremities, resembling mice lacking the farnesylated CAAX protein prelamin A. Prelamin A processing was defective both in fibroblasts lacking Zmpste24 and in fibroblasts lacking the CAAX carboxyl methyltransferase Icmt but was normal in fibroblasts lacking the CAAX endoprotease Rce1. Muscle weakness in Zmpste24(-/-) mice can be reasonably ascribed to defective processing of prelamin A, but the brittle bone phenotype suggests a broader role for Zmpste24 in mammalian biology.

Age Factors↗

PubMed2001

Mobility impairment, muscle imbalance, muscle weakness, scapular asymmetry and shoulder injury in elite volleyball athletes.

BACKGROUND: The aim of this study was to evaluate the relationship between shoulder mobility, rotator muscles' strength and scapular symmetry, and shoulder injuries and/or pain in elite volleyball athletes. METHODS: An isokinetic shoulder muscle strength test, which was performed at speeds of 60/sec and 180/sec, and shoulder mobility and scapula lateral slide tests were conducted bilaterally on 16 subjects, who represented the England elite volleyball players. The subjects also prospectively completed monthly questionnaires during the competition season to report on their shoulder condition. RESULTS: The results showed that the active range of shoulder internal rotation and concentric external rotators' strength in the dominant arm were significantly less, than in the non-dominant arms, but the internal rotators were significantly stronger in both concentric and eccentric tests at both testing speeds. Seven of 16 subjects indicated overt shoulder injury or pain during their training season, nine subjects had shoulder mobility impairment, seven had muscle imbalance, 13 had relative muscle weakness and five had scapular asymmetry. The association between shoulder muscle strength imbalance (eccentric external < concentric internal) of rotators in the dominant arm and shoulder injuries was statistically significant (Fisher's exact test, p<0.05). CONCLUSIONS: We conclude that rotator muscle strength imbalance may play an important role in shoulder injuries in high-level volleyball players.

Adult↗

PubMedDate not supplied

Treatment of "permanent" muscle weakness in familial Hypokalemic Periodic Paralysis.

Three patients with Hypokalemic Periodic Paralysis (HOPP)-associated progressive interattack muscle weakness, who became unresponsive or worsened by acetazolamide, responded favorably to dichlorophenamide, a more potent carbonic anhydrase inhibitor. Dichlorophenamide in single-blind placebo-controlled trials, considerably improved functional strength in two of the patients and had a moderate but definite effect in the third. Muscle groups graded 4/5 (MRC scale)returned to normal; very weak (0-3/5) atrophic muscles, improved to a minor degree. In one patient with acetazolamide-resistant paralytic attacks, dichlorophenamide also diminished the frequency and severity of the acute attacks. Dichlorophenamide had, in the present study, less effect than acetazolamide in reducing serum HCO3(-) and elevating Cl-. Its effectiveness may be related to the degree of sensitivity of certain HOPP patients to alterations of Cl- and/or HCO3(-) serum levels or to a different action of the drug unrelated to carbonic anhydrase inhibition or acidosis. Dichlorophenamide should be considered as an alternate to acetazolamide in the treatment of patients with HOPP-associated interattack muscle weakness who have become unresponsive or worsened by acetazolamide.

Adult↗

PubMed2006

Muscle weakness as presenting symptom of osteogenesis imperfecta.

A young boy presented with severe muscle weakness of his legs at the age of 2 years. Muscle morphology and computer tomography imaging findings were compatible with a metabolic myopathy. Additional investigation showed an osteopenic skeleton and signs of healing fractures. A skin biopsy showed an abnormal electrophoresis pattern of collagen, consistent with a variant of osteogenesis imperfecta. The patient improved with intravenous treatment with pamidronate.

Bone Density Conservation Agents↗

PubMed2006

A case study of gait compensations for hip muscle weakness in idiopathic inflammatory myopathy.

BACKGROUND: The purpose of this case series was to quantify different strategies used to compensate in gait for hip muscle weakness. METHODS: An instrumented gait analysis was performed of three females diagnosed with idiopathic inflammatory myopathies and compared to a healthy unimpaired subject. Lower extremity joint moments obtained from the gait analysis were used to drive an induced acceleration model which determined each moment's contribution to upright support, forward progression, and hip joint acceleration. FINDINGS: Results showed that after midstance, the ankle plantar flexors normally provide upright support and forward progression while producing hip extension acceleration. In normal gait, the hip flexors eccentrically resist hip extension, but the hip flexor muscles of the impaired subjects (S1-3) were too weak to control extension. Instead S1-3 altered joint positions and muscle function to produce forward progression while minimizing hip extension acceleration. S1 increased knee flexion angle to decrease the hip extension effect of the ankle plantar flexors. S2 and S3 used either a knee flexor moment or gravity to produce forward progression, which had the advantage of accelerating the hip into flexion rather than extension, and decreased the demand on the hip flexors. INTERPRETATION: Results showed how gait compensations for hip muscle weakness can produce independent (i.e. successful) ambulation, although at a reduced speed as compared to normal gait. Knowledge of these successful strategies can assist the rehabilitation of patients with hip muscle weakness who are unable to ambulate and potentially be used to reduce their disability.

Acceleration↗

PubMed1986

Pronator muscle weakness in functional instability of the ankle joint.

Functional instability, i.e., recurrent sprains or a feeling of "giving way" of the ankle, is common after ankle sprains. These patients have been supposed to have peroneal muscle weakness based on manual methods for measuring muscle strength. We have confirmed this theory by an isokinetic method for testing pronator muscle strength. Pronator muscle weakness on the affected side was found among patients with unilateral functional instability of the ankle joint. Impaired postural control was demonstrated by stabilometry with the patient standing on either foot.

Adolescent↗

PubMed2001

Quadriceps muscle weakness following acute hemiplegic stroke.

OBJECTIVE: To determine whether quadriceps muscle weakness develops on the side ipsilateral to the brain lesion in the first week following acute ischaemic hemiplegic stroke. DESIGN: A prospective study of muscle strength. SETTING: Acute stroke unit (ASU) in a teaching hospital. SUBJECTS: Ten patients admitted within 48 hours of stroke onset, and 10 healthy age-matched controls. INTERVENTIONS: Repeat nonvolitional measurements of quadriceps muscle strength of the unaffected limb in patients and the right leg in normal subjects using magnetic femoral nerve stimulation (MS), prospectively one week apart. In addition the level of voluntary activation was assessed during a maximum voluntary contraction (MVC) manoeuvre. The Trunk Control Test (TCT) was measured in the patients. RESULTS: The median (95% confidence interval, (CI)) baseline quadriceps twitch tension (Tw Q) and MVC in the control group were 9.4 kg (6.1-12.5 kg) and 37.2 kg (23.8-54.6 kg), and in the stroke group were 7.6 kg (4.4-9.9 kg) and 12.15 kg (7.9-30.8 kg). The median (95% CI) change in Tw Q and MVC respectively between baseline and one week later were 1.75% (-9.8 to 8%) and 5.45% (-15.1 to 22.7%) (NS) in the control group and -16.2% (-6 to -25.9%) and -30.45% (0 to -78.6%) (p < 0.01) in the stroke patients. There was a significant correlation between the percentage fall in Tw Q and both change in TCT (rs = 0.83, p < 0.01) and percentage change in body weight (rs = 0.83, p < 0.01). CONCLUSION: In the first week after acute hemiplegic stroke, weakness develops in the unaffected leg.

Aged↗

PubMed1990

Myotonic dystrophy: quantification of muscle weakness and myotonia and the effect of amitriptyline and exercise.

The purpose of this study was to quantify the degree of muscle weakness and myotonia in 12 patients with myotonic dystrophy (MD), and to quantitatively determine the effects of a four- to six-month therapeutic trial of amitriptyline. Patients had exercised with weights for one or more years. Some had shown initial improvement in muscle strength, but had reached a plateau; others had not improved when the study began. Muscle weakness was quantified by comparing the five-second maximum voluntary contraction (MVC) in newtons (N) per kg (body weight) of 12 patients and 20 healthy subjects. Knee extensor, elbow flexor, and first dorsal interosseous (FDI) muscles were compared. Myotonia was quantified by measuring relaxation times (RTs) at the end of the five-second MVC produced by FDI, as the time taken for the MVC to decrease by 50% and 75% (referred to as 1/2 and 3/4RT). The results were as follows: (1) the mean muscle strength of each of the three muscles of the patients was significantly (p less than .001) reduced compared with healthy subjects; and (2) 1/2 and 3/4RT means of the patients (vs healthy subjects) were significantly prolonged (p less than .01). Eight of the patients participated in a therapeutic trial of amitriptyline. Therapeutic effects were quantified by measuring muscle strength, 1/2 and 3/4RT, and percent change in evoked muscle action potential (MAP) from the FDI muscle after a ten-second MVC, to determine change in excitability. Mean muscle strength of FDI improved from .27 to .33N/kg, (p less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗

PubMed2003

Respiratory muscle weakness and anorexia nervosa.

BACKGROUND: Nutritional recovery in anorexia nervosa (AN) is associated with improved exercise tolerance. METHOD: We describe the investigation of a male with AN. Despite nutritional recovery, he complained of impaired exercise tolerance. RESULTS: Respiratory muscle weakness was demonstrated as the cause of the impaired exercise tolerance. DISCUSSION: Weakness of the muscles of respiration results from prolonged malnutrition. The diaphragmatic muscle may be slower to recover than other muscles. This can cause impaired exercise tolerance due to shortness of breath on exertion, despite nutritional recovery.

Anorexia Nervosa↗

PubMed2005

Cervical muscles weakness in chronic whiplash patients.

BACKGROUND: Isometric cervical strength has been used for assessing the severity of cervical spine pathologies. However there is a conspicuous dearth of information relating to cervical strength data in patients suffering from chronic whiplash. Therefore the objective of this study was to compare absolute and ratio-based isometric cervical strength scores in chronic whiplash patients with reported corresponding scores in healthy subjects. METHODS: Isometric cervical strength was measured in the directions of flexion, extension, right and left lateral flexion in 97 patients, 51 women and 46 men, using a wall-mounted dynamometer. FINDINGS: Compared to published values of normal subjects, whiplash patients suffered sharp reductions of about 90% in both genders and in all directions. The consistency of the isometric cervical strength scores as indicated by the mean coefficient of variation was relatively low, 17% and 20% in men and women respectively. The flexion/extension strength ratio ranged 0.8--0.9, slightly higher than the reported range for normal subjects. This ratio was highly correlated (r=0.91, P=0.01) with the mean coefficient of variation in a subgroup of 9 patients. INTERPRETATION: In the absence of an obvious reason such as sever atrophy or grossly dysfunctional neurological control the indicated weakness of the cervical muscles may be associated with learned pain avoidance behavior which is typical among this group of patients.

Adult↗

PubMed1983

Hypoglycemia, hepatic dysfunction, muscle weakness, cardiomyopathy, free carnitine deficiency and long-chain acylcarnitine excess responsive to medium chain triglyceride diet.

Fraternal twins who had fasting hypoglycemia, hypoketonemia, muscle weakness, and hepatic dysfunction are reported. The hepatic dysfunction occurred only during periods of caloric deprivation. The surviving patient developed a cardiomyopathy. In this sibling, muscle weakness and cardiomyopathy were markedly improved by a diet high in medium chain triglycerides. There was a marked deficiency of muscle total carnitine and a mild deficiency of hepatic total carnitine. Unlike patients with systemic carnitine deficiency, serum and muscle long-chain acylcarnitine were elevated and renal reabsorption of carnitine was normal. It was postulated that the defect in long-chain fatty acid oxidation in this disorder is caused by an abnormality in the mitochondrial acylcarnitine transport. Detailed studies of the cause of the hypoglycemia revealed that insulin, growth hormone, cortisol, and glucagon secretion were appropriate and that it is unlikely that there was a major deficiency of a glycolytic or gluconeogenic enzyme. Glucose production and alanine conversion to glucose were in the low normal range when compared to normal children in the postabsorptive state. The hypoglycemia in our patients was probably due to a modest increase in glucose consumption, secondary to the decreased oxidation of fatty acids and ketones, alternate fuels which spare glucose utilization, plus a modest decrease in hepatic glucose production secondary to decreased available hepatic energy substrates.

Cardiomyopathies↗

PubMed1988

Hypophosphatemia-associated respiratory muscle weakness in a general inpatient population.

Although hypophosphatemia has been implicated as a cause of respiratory failure, its impact on respiratory muscle function in patients hospitalized for other reasons remains to be determined. Maximal inspiratory pressures (MIP) and maximal expiratory pressures (MEP) were measured at the bedside in 23 hospitalized patients with serum phosphate levels less than 2.5 mg/dl, and these measurements were repeated daily during phosphate repletion until serum phosphate levels reached the normal range. A control group consisted of 11 normophosphatemic inpatients. Sixteen of 23 hypophosphatemic patients, but none of the control patients (p less than 0.001), exhibited respiratory muscle weakness, defined as a MIP less than 40 cm H2O or a MEP less than 70 cm H2O. The mean initial MIP and MEP values were also significantly lower for the hypophosphatemic group. A significant correlation existed between initial phosphate level and initial MIP value (r = 0.50, p less than 0.02). With phosphate repletion, mean +/- SD MIP increased from -37 +/- 26 cm H2O to -49 +/- 24 cm H2O (p less than 0.003) and MEP from 60 +/- 20 cm H2O to 69 +/- 19 cm H2O (p less than 0.02). It is concluded that respiratory muscle weakness is common among hypophosphatemic patients and improves with phosphate repletion.

Aged↗