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PubMed1992

[Reducing body myopathy--a case report].

A 2-year-old girl with reducing body myopathy was reported. She had no family history of neuromuscular disease. She developed normally with no delay in milestones during infancy. She had no muscle weakness or hypotonia up to 2 years of age when she received mumps vaccination. Three days after the injection, she was first noticed to have limb muscle weakness. The muscle weakness progressed rapidly with increasing difficulty in gait and raising the upper arms, particularly the left. Four months later, she had difficulty in keeping her head up and could no longer climb the stairs. On physical examination, she had proximal dominant generalized muscle weakness, with a preferential neck muscle involvement. She walked waddlingly and stood up with Gowers' maneuver. Facial and ocular muscles were intact. No dysarthria, dysphagia or respiratory difficulty was noted. EMG showed myopathic pattern. Serum creatine kinase level was moderately elevated to 739 IU/l. In the biopsied left biceps muscle, there was marked variation in fiber size, but no apparent necrotic or regenerating fibers. The most striking feature was the presence of numerous eosinophilic inclusions which reduced nitroblue tetrazolium (NBT) and were, therefore, stained dark with menadione-linked alpha-glycerophosphate dehydrogenase even without the substrate of menadione, showing the histochemical characteristics of "reducing" body. The bodies were predominantly seen in fibers with disorganized intermyofibrillar networks and with high acid phosphatase activity. On electron microscopy, the reducing bodies consisted of fine granular material with the similar electron density to the chromatin granules and were located mostly around the degenerated nuclei, suggesting the nuclear degeneration playing a role in forming the reducing bodies.(ABSTRACT TRUNCATED AT 250 WORDS)

Child, Preschool↗

PubMed2001

Juvenile dermatomyositis in Thai children.

Juvenile dermatomyositis is a rare, chronic multisystemic inflammatory disorder of unknown etiology, characterized by a typical skin rash and proximal muscle weakness. A retrospective study from the medical records of patients diagnosed as juvenile dermatomyositis was performed at Queen Sirikit National Institute of Child Health from 1988 to 1998. There were seven cases of juvenile dermatomyositis diagnosed according to the criteria of Bohan and Peter. Six cases were female and one case was male. The age of diagnosis ranged from 2.5 years to 11 years. (mean age was 7 +/- 3.6 years). The presenting symptoms were muscle weakness (6 cases), muscle pain (2 cases) and skin rashes (4 cases). All of the patients developed proximal muscle weakness of the lower extremities varying from grade 3 to grade 4. The cutaneous manifestations were heliotrope signs (6 cases), gottron's papules (2 cases), photosensitivity (2 cases) and calcinosis cutis (4 cases). Electromyography (EMG) was performed in 6 cases and revealed typical change of myopathic type. Elevated muscle enzymes were noted in all cases. Muscle biopsy was performed in 6 cases and was compatible with myositis. Oral prednisolone (1-2 mg/kg/day) was given in 6 cases and the muscle weakness improved. There was no mortality in this study. Four cases developed calcinosis cutis 1 to 3 years after muscle weakness and did not respond to any treatment. In conclusion, juvenile dermatomyositis is a disease which causes chronic disability in children. Early diagnosis and treatment can prevent morbidity and mortality. Calcification at the skin usually occurs after the onset of muscle weakness several months to years after diagnosis.

Child↗

PubMed2002

Clinical spectrum of inflammatory myositis in South India--a ten year study.

OBJECTIVE: To describe the clinical spectrum of inflammatory myopathies at a referral hospital in South India. METHODS: Patients were assessed for the pattern of muscle involvement, for the presence of arthritis, Raynaud's phenomenon, interstitial lung disease (ILD) and cardiac involvement. Muscle enzymes, electromyogram (EMG) and muscle biopsies were done. RESULTS: Eighty seven patients with inflammatory myopathies were encountered over 10 years. These included 24 with adult polymyositis, 26 with adult dermatomyositis, one with amyopathic dermatomyositis, five with juvenile myositis, one with dermatomysitis following carcinoma breast and 30 with overlap with other connective tissue diseases. There was a female preponderance (M:F = 1:2.35) except in juvenile myosits group (M:F = 1.5:1). The mean age of onset in years was 33.26 in adult polymyositis, 35.03 in adult dermatomyositis, 7.4 in juvenile dermatomyositis, 42 in malignancy-associated dermatomyositis and 25.51 in the overlap group. Proximal muscle weakness was seen in 98.8% patients, dysphagia in 33.3%, distal muscle weakness in 12.5%, respiratory muscle weakness in 9.2% and dysphonia in 4.6%. Other features included arthritis 35.63%, interstitial lung disease (ILD) 9.2%, Raynaud's 5.7%, myocarditis 4.6% and conduction disturbances 1.15%. Eleveated muscle enzymes were seen in 85.1% patients. Eletromyogram was positive in 66.6%. Muscle biopsy was positive in 85.29%. Anti-nuclear antibody was positive in 67.24%. All received steroids, non-responders needed methotrexate (13 patients) or azathioprine (11 patients). Death occurred in 10 (seven with dermatomyositis predominantly due to respiratory involvement and three with overlap). CONCLUSION: There was female preponderance except in juvenile myositis group. Proximal muscle weakness was the commonest feature. ILD was the commonest respiratory problem, while myocarditis was the commonest cardiac problem seen. Response to therapy and prognosis in polymyositis were good with no mortality during the study period. Death in the dermatomyositis group was mainly due to respiratory involvement.

Adolescent↗

PubMed2006

Muscle force and fatigue in patients with sepsis and multiorgan failure.

INTRODUCTION: Neuromuscular abnormalities are found frequently in sepsis and multiorgan failure (MOF). Surprisingly, however, there are no data on maximum skeletal muscle force and fatigue in these patients. OBJECTIVES: To test the research hypotheses that adductor pollicis (AP) force would be lower in patients with sepsis, whereas fatigue would not differ between patients and immobilized but not infected volunteers. DESIGN AND SETTING: Prospective study; university intensive care unit and laboratory. PATIENTS: Patients with sepsis and MOF (sequential organ failure assessment (SOFA) score >10) and healthy volunteers. INTERVENTIONS: Fatigue was evoked during 20[Symbol: see text]min of intermittent tetanic ulnar nerve stimulation achieving 50% of maximum AP muscle force. MEASUREMENTS AND RESULTS: We measured evoked AP muscle force and fatigue, and compound muscle action potential (CMAP), and performed standard electrophysiological tests in 13 patients, and in 7 volunteers before and after immobilization. Maximum force (20+/-16 vs 65+/-19N; p<0.01) and CMAP (3.6+/-2.5 vs 10+/-2.5 mV; p<0.05) were markedly decreased in patients; however, fatigue and ulnar nerve conduction velocity did not differ from volunteers, and a decrement of CMAP was not observed with nerve stimulation frequencies up to 40 Hz. All patients with critical illness polyneuropathy, and an additional 50% of those without, had significant muscle weakness. CONCLUSION: Peripheral muscle force is markedly decreased in sepsis, without evidence for an increased fatigability. Muscle weakness was most likely due to a sepsis-induced myopathy and/or axonal neuropathy, and was not the result of an immobilization atrophy.

Action Potentials↗

PubMed2004

Anti-signal recognition particle autoantibody in patients with and patients without idiopathic inflammatory myopathy.

OBJECTIVE: To determine the long-term outcome and associated clinical, serologic, and pathologic features in a cohort of patients with connective tissue disease (CTD) and the anti-signal recognition particle (anti-SRP) autoantibody. METHODS: Sera and clinical data were collected prospectively from consecutive adult patients with polymyositis (PM; n = 134), dermatomyositis (n = 129), or other CTDs (predominantly systemic sclerosis [SSc; n = 790]). Patients were first evaluated during 1973-2001. RESULTS: Nineteen patients with the anti-SRP autoantibody were identified, 16 (84%) of whom had pure PM and 3 (2 with SSc and 1 with antisynthetase syndrome) had yet to develop features of myositis after a mean followup of 4.5 years (range 2.5-6 years). More SRP-positive PM patients had severe proximal muscle weakness (50%) and muscle atrophy (67%) at initial presentation compared with antisynthetase-positive PM controls. Cardiac involvement occurred in only 2 of 16 SRP-positive PM patients (13%), and interstitial lung disease was noted in 3 of 13 SRP-positive PM patients (23%) and in the 3 SRP-positive nonmyositis patients. There was a relative lack of inflammation in muscle biopsy specimens from the SRP-positive PM cohort. Other autoantibodies in the SRP-positive patients included Ro/SSA (4 patients), Th/To (1 patient), and anti-PL-12 (1 patient). Survival in the SRP-positive PM patients was comparable with that seen in the cohort of SRP-negative PM patients. CONCLUSION: The anti-SRP autoantibody is not specific for PM. Severe muscle weakness and atrophy were prominent features in PM patients with anti-SRP. Cardiac involvement was less common and survival was better in patients with anti-SRP than has previously been reported.

Adult↗

PubMed2001

Reference values of maximum isometric muscle force obtained in 270 children aged 4-16 years by hand-held dynamometry.

Since muscle force and functional ability are not related linearly; maximum force can be reduced while functional ability is still maintained. For diagnostic and therapeutic reasons loss of muscle force should be detected as early and accurately as possible. Because of growth factors, maximum muscle force in children varies with age, which makes detection of force loss difficult. The purpose of this study was to establish reference values for muscle force in children aged 4-16 years, obtained by hand-held dynamometry in 11 muscle groups. In boys muscle force was predicted best by weight whereas in girls weight and age were best predictors. At age 14 boys become significantly stronger for nearly all tested muscle groups. These age-related reference values can be used to quantify muscle weakness in individual muscle groups in children aged 4-16 years and to evaluate the effects of therapy.

Adolescent↗

PubMedDate not supplied

Intranuclear rod myopathy, a rare and morphologically striking variant of nemaline rod myopathy.

A 4-year-old boy with muscle weakness underwent skeletal muscle biopsies. Light microscopy showed distinct eosinophilic inclusions within the majority of muscle cell nuclei, but none in the cytoplasm. Electron microscopy revealed crystalline, round to rod-shaped inclusions in the muscle cell nuclei. The inclusions stained positively for alpha-actinin. Intranuclear inclusions identical to those seen here have been described in rare cases of nemaline rod myopathy, though almost always together with classic intracytoplasmic rods. This case illustrates the importance of electron microscopy in the diagnosis of rare myopathies and in the characterization of cellular inclusions of unknown origin.

Biomarkers↗

PubMed2007

Autopsy case of desminopathy involving skeletal and cardiac muscle.

Desminopathy is a familial or sporadic skeletal and cardiac muscular dystrophy caused by mutation in the desmin gene. Desmin-reactive deposits in the affected muscles are the morphological hallmarks of this disease. Herein is reported an autopsy case of a 57-year-old Japanese man with adult-onset skeletal muscle weakness and atrioventricular (A-V) conducting block, with a missense A337P mutation in exon 5 of the desmin gene. Disease onset occurred when the patient was 45 years old. The initial presentation was lower limb weakness, and the weakness progressed to the upper limbs. When the patient was 51 years old, a cardiac pacemaker was implanted due to complete A-V block. When the patient was 53 years old, respiratory insufficiency occurred due to weakness of respiratory muscles, and the patient died at the age of 57 years. On autopsy, intrasarcoplasmic desmin-immunoreactive deposits were identified in the skeletal and cardiac muscle, and abnormal accumulations of granulofilamentous material were identified at the ultrastructural level. In the cardiac conducting system, calcification was observed at the bundle of His, and sporadic calcium deposits were observed at the left and right bundle branches.

Autopsy↗

PubMed2024

An insight into the causal relationship between sarcopenia-related traits and venous thromboembolism: A mendelian randomization study.

BACKGROUND: As a geriatric syndrome, sarcopenia has a high prevalence in the old population and represents an impaired state of health with adverse health outcomes. A strong clinical interest in its relationship with venous thromboembolism (VTE), which is a complex trait disease with a heterogeneous annual incidence rate in different countries, has emerged. The relationship between sarcopenia and venous thromboembolism has been reported in observational studies but the causality from sarcopenia to VTE remained unclarified. We aimed to assess the causal effect of sarcopenia on the risk of VTE with the two-sample Mendelian randomization (MR) method. METHODS: Two sets of single-nucleotide polymorphisms (SNPs), derived from two published genome-wide association study (GWAS) meta-analyses and genetically indexing muscle weakness and lean muscle mass separately, were pooled into inverse variance weighted (IVW), weighted median and MR-Egger analyses. RESULTS: No evidence was found for the causal effect of genetically predicted muscle weakness (IVW: OR = 0.90, 95% CI = 0.76-1.06, p = 0.217), whole body lean mass (IVW: OR = 1.01, 95% CI = 0.87-1.17, p = 0.881) and appendicular lean mass (IVW: OR = 1.13, 95% CI = 0.82-1.57, p = 0.445) on the risk of VTE. However, both genetically predicted whole-body lean mass and appendicular lean mass can causally influence diabetes mellitus (IVW of whole-body lean mass: OR = 0.87, 95% CI = 0.78-0.96, p = 0.008; IVW of appendicular lean mass: OR = 0.71, 95% CI = 0.54-0.94, p = 0.014) and hypertension (IVW of whole-body lean mass: OR = 0.92, 95% CI = 0.87-0.98, p = 0.007; IVW of appendicular lean mass: OR = 0.84, 95% CI = 0.73-0.96, p = 0.013). CONCLUSIONS: Genetically predicted sarcopenia does not causally influence VTE directly, but it might still have an indirect effect on VTE incidence via diabetes mellitus and hypertension.

Humans↗

PubMed2006

Autoimmune thrombocytopenic purpura, autoimmune hemolytic anemia and gastric cancer appeared in a patient with myasthenia gravis.

We report a case of myasthenia gravis (MG) associated with autoimmune thrombocytopenic purpura (AITP) and autoimmune hemolytic anemia (AIHA), and after that gastric cancer appeared. A 51-year-old man began to suffer from fluctuated muscle weakness in 1985. Muscle weaknesses became exacerbated, and he was admitted to our hospital in 1989. He was diagnosed as MG associated with AITP. After a thymectomy (hyperplasia), prednisolone therapy was started, subsequently his condition was satisfactory. In March 1995, he developed severe anemia and icterus. He was diagnosed as Evans' syndrome (AIHA and AITP) with MG. High-doses of immunoglobulin administration improved the anemia, but thrombocytopenia continued. In November 2002, he suffered marked petechia; the platelet count decreased to 1000/microl. Methylprednisolone pulse therapy and platelet transfusion were started. Gastrofiberscopy was performed and biopsy specimens revealed signet cell-type adenocarcinoma. On December 19, 2002, subtotal gastrectomy and splenectomy were performed. After that, his condition has remained satisfactory, without MG symptoms or thrombocytopenia. This is the first such case report in the literature.

Anemia, Hemolytic, Autoimmune↗

PubMed2000

Neurological syndromes following organophosphate poisoning.

Organophosphorous compounds, the anticholinesterases, produce significant morbidity and mortality in India. Although exact estimates are not available, hospital based statistics suggest that nearly half of the admissions to emergency with acute poisoning are due to organophosphates. Following accidental or suicidal exposure, these anticholinesterases lead to three well defined neurological syndromes i.e. initial life threatening acute cholinergic crisis which often requires management in intensive care unit, intermediate syndrome in which cranial nerve palsies, proximal muscle weakness and respiratory muscle weakness are common and patients often require respiratory support and delayed organophosphate induced polyneuropathy. In addition to these three classical neurological syndromes following acute exposure and in some following low dose chronic exposure, several neurobehavioural changes have been observed and these have been termed together as 'chronic organophosphate induced neuropsychiatric disorders' (COPIND). Organo-phosphate compounds produce significant pesticide related illness in developing countries. There is, thus, a need to determine exact extent of the problem and to develop appropriate strategies to manage these cases with available resources in these countries.

Cholinesterase Inhibitors↗

PubMed2006

Neuromuscular disease causing acute respiratory failure.

In the developed world, Guillain-Barré syndrome and myasthenia gravis account for the majority of cases of acute respiratory failure associated with neuromuscular disease. The 4 components that contribute to respiratory failure are upper-airway dysfunction, inspiratory-muscle weakness, expiratory-muscle weakness, and the pulmonary complications associated with these conditions. Careful observation and objective monitoring are essential to determine the appropriate timing of intubation and mechanical ventilation. Pulmonary function tests that can help predict the need for mechanical ventilation include vital capacity, peak inspiratory pressure, and peak expiratory pressure. The morbidity and mortality of patients who require mechanical ventilation are not insubstantial. This paper will review the mechanisms underlying acute respiratory failure, the clinical assessment of patients, the predictors of the need for mechanical ventilation, and the intensive-care-unit morbidity and mortality of patients with Guillain-Barré syndrome or myasthenia gravis.

Critical Care↗

PubMed2000

Herpes zoster infection complicated by motor paralysis.

We reviewed a total of 1,432 patients diagnosed with cutaneous herpes zoster at Hyogo College of Medicine Hospital between 1989 and 1997 for epidemiologic assessment and outcome in patients with zoster paralysis referred for rehabilitation. Of the 1,432 herpes zoster patients (624 males and 808 females, mean age 54.3 years), 12 were referred to our department of rehabilitation medicine for muscle weakness: one had myelitis, and eleven others had lower motor neuron damage. Except for one 43-year-old man with myelodysplastic syndrome, all the lower motor neuron deficit patients were over 60 years of age. Involved myotomes were more widespread than involved dermatomes in eight patients. Electromyography in four patients demonstrated denervation of involved muscles. Five patients experienced complete or near complete recovery from their muscle weakness. The muscle weakness related to herpes zoster was occasionally diagnosed by electromyography as motor neuron damage. Manifestations of motor neuron complications were not noticed but might in fact be more common than was the clinical muscle weakness.

Adolescent↗

PubMed1985

Muscle acetylcholine receptor loss in murine experimental autoimmune myasthenia gravis: correlated with cellular, humoral and clinical responses.

An extensive analysis of the relationship between immunological parameters and clinical responses and biochemical loss of muscle acetylcholine receptors (AChR) was performed in murine experimental autoimmune myasthenia gravis. The onset of clinical muscle weakness correlated strongly with the onset of significant muscle AChR loss. Mice with clinical muscle weakness had greater amount of muscle AChR loss. There was no correlation between the concentration of anti-AChR antibodies and the presence of clinical muscle weakness or amount of muscle AChR loss. However, the kinetics of autoantibody response correlated well with that of muscle AChR loss.

Autoantibodies↗

PubMed1997

Classification criteria for the idiopathic inflammatory myopathies.

Inasmuch as the clinical features of the idiopathic inflammatory myopathies are not easily differentiated from those of other similar rheumatic and neurologic conditions, diagnosis is often difficult. Various classification criteria for polymyositis and dermatomyositis have been suggested by a number of investigators. The most commonly accepted and used criteria include symmetric proximal muscle weakness, serum elevations of muscle enzymes, the classic electromyographic and muscle biopsy findings of inflammatory myopathy, and the typical skin rash of dermatomyositis. Although these criteria are clinically useful, they can result in misdiagnoses and inappropriate therapies. They also result in heterogeneous patient groups being selected for clinical and laboratory studies. Furthermore, they do not include recent findings related to the myositis-specific autoantibodies and magnetic resonance imaging of muscle that have been found to be important adjuncts in assessing patients with muscle weakness or elevations of muscle enzymes. A modification to the Bohan and Peter criteria is proposed to include myositis-specific autoantibodies and magnetic resonance imaging. This proposal could initiate productive discussions and investigations of the sensitivity and specificity of new classification criteria for myositis and could ultimately enhance our treatment capabilities.

Autoantibodies↗

PubMed2001

A deceptive case of amyloid myopathy: clinical and magnetic resonance imaging features.

Amyloid myopathy is a well-described, increasingly recognized clinical entity. Similar to inflammatory myopathies, amyloid myopathy presents with proximal muscle weakness and can be associated with elevated levels of muscle enzymes. We report the case of a 58-year-old woman who, at presentation to her physician with proximal muscle weakness and congestive heart failure, was antinuclear antibody positive and had muscle biopsy findings "consistent with inflammatory myopathy." She was referred to Johns Hopkins University Medical Center with the diagnosis of polymyositis. Further investigation revealed a monoclonal gammopathy, a unique patterning of subcutaneous fat reticulation and hypodense bone marrow changes on magnetic resonance imaging (MRI), and an endocardial biopsy sample that was positive for light chain amyloid deposition. Paraffin sections of the muscle biopsy sample from the time of her original presentation were obtained, and Congo red staining showed diffuse amyloid deposition throughout the sample, but no inflammation. This case not only illustrates that proximal muscle weakness due to primary amyloid myopathy (as found in light chain amyloidosis and transthyretin amyloidosis) can mimic that of polymyositis, but also shows that unique findings on MRI can alert the clinician to the diagnosis of amyloidosis prior to muscle biopsy.

Amyloidosis↗

PubMed2002

Botulinum neurotoxin serotypes A and B preparations have different safety margins in preclinical models of muscle weakening efficacy and systemic safety.

This preclinical study compared the muscle weakening efficacy, duration, and safety margin of the recently approved botulinum toxin type B (BTX-B; Myobloc/Neurobloc) to botulinum toxin type A (BTX-A; BOTOX((R))). Mice received a single hind limb intramuscular injection of BTX-B (1-150U/kg) or BTX-A (1-120U/kg). An observer who was masked to treatment assessed the magnitude and duration of muscle weakening efficacy on a 0-4 scale using the digit abduction scoring assay. Safety margins were determined as the ratio of the IM median lethal dose to the IM dose that produced half-maximal muscle weakness in the DAS. BTX-A produced muscle weakness at lower doses than BTX-B (IM ED(50): 6.2+/-0.6 vs. 20.8+/-1.4U/kg, respectively) (p<0.0001). BTX-A at 29U/kg and BTX-B at 67U/kg produced comparable peak DAS scores of approximately 4 indicating maximal muscle weakness. At these doses, the duration of BTX-A was longer, with a return to baseline by day 36 compared to a return to baseline by day 14 with BTX-B. The mean dose that was lethal in 50% of mice was lower for BTX-A than BTX-B (81.4+/-3.5 vs. 104.6+/-1.9U/kg, respectively) (p<0.001) and the safety margin was higher (13.9+/-1.7 vs. 5.4+/-0.3, respectively (p<0.001). These results indicate that the BTX-A:BTX-B dose ratio for muscle weakening efficacy is different from the ratio for systemic effects following IM injections and suggest that no single dose ratio is adequate to compare these preparations. The in vivo differences found are consistent with the different clinical profiles reported for these two products.

Animals↗

PubMed1977

Acetylcholine receptor protein. Neuromuscular transmission in immunized rabbits.

Rabbits injected with purified acetylcholine (ACh) receptor protein produce antibodies against the receptor and develop generalized muscle weakness. The compound muscle action potentials show a decremental fall in amplitude with repetitive nerve stimulation. Both the weakness and the decrement is counteracted by reversible cholinesterase inhibitors. Intracellular recordings from muscle endplates show that the amplitude of the miniature end-plate potentials is considerably reduced. A reduced binding of neurotoxin to muscles from immunized rabbits was observed. Nerve impulses release a normal number of ACh packages (quanta) from the motor nerve terminals. The muscle weakness in immunized rabbits thus has the same features as the muscle weakness in myasthenia gravis and may be a good animal model of myasthenia gravis.

Acetylcholine↗