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Recovery from disuse osteopenia coincident to restoration of muscle strength in mdx mice.

The objective of this study was to compare the tibial structure and the strength of the tibia during muscle weakness and after recovery in mdx mice (which demonstrate X-linked muscular dystrophy and subsequent muscle regeneration) and age-matched control mice. The extent of disuse atrophy produced by muscle weakness and recovery following restoration of normal muscle strength could then be determined. The tibiae adjacent to weakened tibialis anterior muscles of 4-week-old mdx mice had significantly reduced radiographic density (p < 0.05) and cortical thickness (p < 0.001), and increased porosity (p < 0.001) compared to age-matched controls, suggesting development of disuse osteopenia. Significantly less force was required to break mdx tibiae than age-matched control tibiae (p < 0.05). In addition, Sharpey's fiber density was reduced (p < 0.001), suggesting a weakened attachment of the tibialis anterior muscle to bone. At 12 weeks, during the period of muscle regeneration, mdx tibial cortical thickness (p < 0.001) and porosity (p < 0.01) remained significantly lower, but percent calcium and Sharpey's fiber and radiographic densities were significantly greater (p < 0.001) than in age-matched controls, suggesting that bone mineralization and muscle attachment strength had increased to above normal levels in parallel with recovery of strength by the attached muscle. By 18 weeks, mdx tibial cross-sectional area, cortical thickness, and porosity remained significantly less (p < 0.001) than normal. Although Sharpey's fiber density was greater than in age-matched controls (p < 0.001) by 18 weeks, mdx tibial percent calcium (p < 0.005) and Sharpey's fiber density (p < 0.001) were significantly reduced from levels in 12-week-old mdx animals. There was significantly less deformation of the tibia prior to fracture in mdx than control tibiae at 18 weeks of age, suggesting tibial brittleness. Thus, at the site of attachment of mdx muscle to osteopenic bone, the remodelling which accompanies recovery of muscle strength is atypical, and produces an attachment of greater strength than function appears to require. These observations suggest that data are needed regarding bone mass and muscle-bone attachments in humans with disuse osteopenia, DMD, and other neuromuscular diseases.

Animals↗

PubMed2000

Sarcoidosis and dermatomyositis in a patient with hemoglobin SC. A case report and literature review.

Although sarcoidosis has occasionally been associated with hemoglobinopathies, its association with dermatomyositis is extremely rare. A 24 y/o African American male with hemoglobin SC disease developed proximal weakness. He had heliotrope rash, muscle weakness, elevated serum CK, myositis by EMG, and no malignancy. A muscle biopsy confirmed dermatomyositis. Two years later, he was hospitalized with constitutional and respiratory symptoms and parotid enlargement. Chest X-ray and CT scan showed diffuse micronodular infiltration in both lungs and mediastinal lymphadenopathy. A transbronchial lung biopsy revealed non-caseating granulomata consistent with sarcoidosis. AFB and fungal stains and cultures were negative. Thus, in this case, sarcoidosis developed after or in association with dermatomyositis. A review of world's literature showed five other non-identical cases of dermatomyositis associated with sarcoidosis.

Adult↗

PubMed1985

Steroid myopathy: incidence and detection in a population with asthma.

Sixty steroid-treated patients with asthma were evaluated for the presence of muscle weakness by use of both manual muscle testing and the Cybex II isokinetic dynamometer. The patients were compared to age and sex-matched sedentary control subjects. Forty-eight percent of the patients (12/25) taking greater than or equal to 40 mg per day of prednisone had hip flexor strength greater than or equal to 2 SD below the mean of age and sex-matched control subjects by Cybex testing (CT). Sixty-four percent of the patients (16/25) taking greater than or equal to 40 mg per day of prednisone were found on manual muscle testing to have hip flexor weakness. Only one patient taking less than 30 mg per day of prednisone was found to have muscle weakness. Biochemical parameters, including CPK, aldolase, SGOT, LDH, and LDH isoenzymes were measured to assess the degree of steroid-induced muscle damage. They neither correlated with the degree of hip flexor weakness as measured by CT, nor did they discriminate between patients receiving small doses and large doses of steroids. Changes in urinary excretion of creatine did not help to confirm the diagnosis of steroid myopathy. Although CT provides an objective means of assessing muscle strength in these patients, at this time no definitive chemical test is available for the diagnosis of steroid myopathy.

Adult↗

PubMed1998

Hyperthyroidism: an unusual case presentation.

Hyperthyroidism is the most common disorder of the thyroid. Patients typically present with complaints consistent with a hypermetabolic state, including nervousness, weight loss, heat intolerance, palpitations, irritability, and tremor. This case report reviews a 34-year-old woman who presented with unilateral upper extremity weakness, weight gain, and an episode of atrial fibrillation, the latter coinciding with a 36-hour lack of sleep and excess alcohol and caffeine intake. Although an extensive neurologic evaluation failed to identify any abnormality, the patient's laboratory analysis revealed elevations in thyroxine (T4) and triiodothyronine (T3) levels with unsuppressed thyroid-stimulating hormone levels. Subsequent treatment with the antithyroid drug methimazole (Tapazole) provided complete relief of symptoms. This case report illustrates how health care providers can be diverted to pursue a neurologic etiology when muscle weakness presents as a unilateral symptom. Plausible alternative causes for muscle weakness and other symptoms are presented.

Adult↗

PubMed2003

Identification of a novel LAMP2 mutation responsible for X-chromosomal dominant Danon disease.

Danon disease (DD) is a rare lysosomal glycogen storage disease with normal acid maltase activity, which is characterised clinically by cardiomyopathy and myopathy, and a variable degree of mental retardation. The causative gene, LAMP2, has been mapped to chromosome Xq24-q25. LAMP2 encodes a lysosome-associated membrane glycoprotein. We identified a novel LAMP2 mutation of the exon 8 splice acceptor site (IVS7-1G --> A) in an affected male and female, which predicts abnormal splicing. Both affected individuals presented solely with hypertrophic cardiomyopathy. Muscle weakness and mental impairment were absent. Diagnosis of Danon disease was established by muscle biopsy, when the male index patient developed transient severe muscle weakness following heart transplantation. Typical biopsy findings were also found in a heart muscle specimen. Demonstration of the LAMP2 mutation in affected male and female siblings is compatible with X-linked dominant inheritance. Danon disease should be actively looked for in cardiomyopathy patients.

Adult↗

PubMed2006

Improvement in survival and muscle function in an mdx/utrn(-/-) double mutant mouse using a human retinal dystrophin transgene.

Duchenne muscular dystrophy is a progressive muscle disease characterized by increasing muscle weakness and death by the third decade. mdx mice exhibit the underlying muscle disease but appear physically normal with ordinary lifespans, possibly due to compensatory expression of utrophin. In contrast, double mutant mice (mdx/utrn(-/-)), deficient for both dystrophin and utrophin die by approximately 3 months and suffer from severe muscle weakness, growth retardation, and severe spinal curvature. The capacity of human retinal dystrophin (Dp260) to compensate for the missing 427 kDa muscle dystrophin was tested in mdx/utrn(-/-) mice. Functional outcomes were assessed by histology, EMG, MRI, mobility, weight and longevity. MCK-driven transgenic expression of Dp260 in mdx/utrn(-/-) mice converts their disease course from a severe, lethal muscular dystrophy to a viable, mild myopathic phenotype. This finding is relevant to the design of exon-skipping therapeutic strategies since Dp260 lacks dystrophin exons 1-29.

Age Factors↗

PubMed2004

Amyloid myopathy presenting with distal atrophic weakness.

Amyloid myopathy is a rare complication of primary amyloidosis usually presenting with proximal muscle weakness. We report a woman with multiple myeloma in whom marked atrophy and weakness of finger flexor muscles were the first manifestations of systemic amyloidosis. Muscle biopsy revealed amyloid angiopathy with deposits of lambda light chains in vessel walls. The recognition of amyloid myopathy is important because clinical symptoms may respond to chemotherapy.

Amyloidosis↗

PubMed1999

Hypoxemia and hypercapnia during exercise and sleep in patients with cystic fibrosis.

BACKGROUND: In patients with cystic fibrosis (CF), it has been proposed that hypoxemia and hypercapnia occur during episodes of stress, such as exercise and sleep, and that respiratory muscle weakness because of malnutrition may be responsible. METHODS: Pulmonary function, respiratory muscle strength, and nutrition were assessed and correlated with the degree of hypoxemia and hypercapnia during exercise and sleep in 14 patients with CF and 8 control subjects. RESULTS: Despite no differences in maximum static inspiratory pressure (PImax) between the two groups, the CF group developed more severe hypoxemia (minimum oxyhemoglobin saturation [SpO2], 89 +/- 5% vs 96 +/- 2%; p < 0.001) and hypercapnia (maximum transcutaneous CO2 tension [PtcCO2], 43 +/- 6 vs 33 +/- 7 mm Hg; p < 0.01) during exercise. Similarly, during sleep, the CF group developed greater hypoxemia (minimum SpO2, 82 +/- 8% vs 91 +/- 2%; p < 0.005), although CO2 levels were not significantly different (maximum PtcCO2, 48 +/- 7 vs 50 +/- 2 mm Hg). Within the CF group, exercise-related hypoxemia and hypercapnia did not correlate with FEV1, residual volume/total lung capacity ratio (RV/TLC), PImax, or body mass index (BMI). Hypoxemia and hypercapnia during sleep correlated with markers of gas trapping (RV vs minimum arterial oxygen saturation [r = -0.654; p < 0.05]), RV vs maximum PtcCO2 (r = 0.878; p < 0.001), and RV/TLC vs maximum PtcCO2 (r = 0.790; p < 0.01) but not with PImax or BMI. CONCLUSION: Patients with moderately severe CF develop hypoxemia and hypercapnia during exercise and sleep to a greater extent than healthy subjects with similar respiratory muscle strength and nutritional status. Neither respiratory muscle weakness nor malnutrition are necessary to develop hypoxemia or hypercapnia during exercise or sleep.

Adult↗

PubMed1989

Muscle histochemistry in myotubular (centronuclear) myopathy.

We report the clinical and histochemical findings in 7 patients with myotubular (centronuclear) myopathy aged from 2 months to 32 years. The clinical symptoms varied from patient to patient. Three patients developed severe muscle weakness and hypotonia with respiratory distress from infancy, and 4 had muscle weakness from 2-5 years of age with no apparent delay in developmental milestones. In addition to an increased number of fibers with centrally placed nuclei, there were 3 other histochemical characteristics of this disorder, i.e., type 1 fiber predominance, type 1 fiber hypotrophy and type 2B fiber deficiency. Other histological findings included a peripheral halo in the sarcoplasm on NADH-TR staining and an increased number of undifferentiated type 2C fibers, indicating a delay in muscle fiber growth and differentiation due to a probable defective neural supply in the developing muscles.

Adult↗

PubMed1999

[A case of Hopkins syndrome with onset at puberty].

The patient was a 15-year-old man who developed weakness of left leg 6 days after an acute asthmatic attack. Neurological examination revealed severe muscle weakness and atrophy at L5-S1 level and mild muscle weakness and atrophy at L2-4 level in the left leg. Deep tendon reflexes were normal in the upper limbs and slightly brisk in the lower limbs except for absence of Achilles tendon reflex on the left. His sensation was normal. Needle EMG revealed neurogenic changes in both the left (L2-S1) and right (L2-4) leg muscles. Motor nerve conduction study of the left tibial and peroneal nerves revealed a marked reduction of amplitude and mild reduction of MCV. F-wave was not evoked in either nerves. Sensory nerve conduction study of the left sural nerve was normal. The titers of anti-viral antibodies in the paired sera showed no significant changes in any viruses examined including echovirus, enterovirus, coxsackievirus and poliovirus type 1, 2 and 3. The serum IgE was elevated (1,300 IU/ml) and mite antigen-specific IgE was strongly positive. Spinal cord MRI revealed no abnormality in either thoracic or lumbar spinal cord. This patient was diagnosed as a rare case of Hopkins syndrome with onset at puberty.

Adolescent↗

PubMed1994

Neuroelectrophysiological evaluation of untreated hyperthyroid patients.

Hyperthyroidism is a common endocrinologic disorder affecting many organ systems. Musculoskeletal and neurological involvement present themselves as fatigue, muscle weakness and paralysis. Electromyography (EMG) is essential for differential diagnosis of muscle weakness. Well defined neuropathy and myopathy have been described in these patients. In the present study 17 hyperthyroid patients were evaluated with electrophysiological tests in addition to physical and neurological examinations and biochemical laboratory studies. Needle EMG, motor and sensory conduction velocities, median and tibial somatosensory evoked potentials (SEP) were studied. For assessment of the activity of disease clinical status, neurological symptom and disability scores and serum T3, T4 and TSH levels were examined. Statistical analysis of neuroelectrophysiological findings of the patient and the control groups yielded meaningful difference in the needle EMG, sensory conduction velocity and evoked potential findings. Abnormalities were observed in 80% of the proximal muscles besides polyphasic potentials that were seen in 20% of the extensor digitorum brevis muscle. Median, ulnar and sural nerve sensory action potential amplitudes were found to be lower than that of the control group. Sural sensory nerve conduction velocity of patients was decreased in 35.5%, prolongation of median SEP latencies and increase in the amplitudes were not however statistically significant. Prolongation of Tibial SEP N1, P2 latencies were seen in 47%, amplitudes of N1 were increased in 88.2%, P2 in 58.8%, N2 in 47%. The thyroid clinical status score was correlated with Tibial SEPs amplitude. These findings suggest the presence of an initial axonal type of mild polyneuropathy. As a conclusion electrophysiological studies can be useful in the diagnosis of asymptomatic polyneuropathy in hyperthyroid patients.

Adolescent↗

PubMed1989

[A case with polymyositis associated with primary hyperparathyroidism].

A 67-year-old woman was admitted to our department because of 5 years' duration of proximal muscle weakness. Serum CK was high, and EMG showed myogenic pattern, and muscle biopsy revealed remarkable inflammatory cells infiltrating around the destroyed muscle fibers. Her muscle weakness and hyperCKemia markedly improved by corticosteroid therapy, suggesting that the diagnosis was compatible with polymyositis (PM). In addition, serum calcium was high and phosphate was low. Serum parathormone level significantly elevated. The findings of diagnostic imaging procedures including echography, scintigraphy, and computed tomography of the parathyroid glands suggested presence of parathyroid adenoma with cystic degeneration in the thyroid tissue. There was only one case report of PM associated with primary hyperparathyroidism (PHP) as the literature referred. In this case, we could not prove direct relationship between PM and PHP. The association might have been coincidental. However, PHP might have played some role in the pathogenesis of muscular involvement, or there might be a similar immunological mechanism as seen between PM and malignancy. It is possible that association of PM and PHP is more frequent than generally considered. It may be necessary to pay more attention to find out the association of PM and PHP.

Adenoma↗

PubMed1990

[Clinical and pathological studies on two patients with adult-onset nemaline myopathy].

Clinical and pathological findings of two patients, a 44-year-old male and a 54-year-old female, with adult-onset nemaline myopathy were described. Both patients showed normal motor development through their childhood; Patient 1 ran fast and was involved in powerful heavy labor until the age of 40, and Patient 2 was in good health until 49, when they began to have progressive muscle weakness. They had no family history of neuromuscular diseases. On neurological examination, they had moderate muscle weakness and atrophy in their limb-girdle and paravertebral muscles. Because paravertebral and neck muscles were preferentially involved, they had difficulty in holding the head straight up. They stood in a lordotic posture. They had neither high-arched palate nor facio-skeletal abnormalities which were common findings in congenital nemaline myopathy. Serum enzymes derived from muscle were normal and needle electromyography showed myogenic and neurogenic changes in both patients. On CT scan of the skeletal muscles, the paravertebral muscles were markedly decreased in density suggesting advanced fat tissue replacement in large areas. In patient 2 who was in more advanced stage, the quadriceps femoris, hamstrings and soleus muscles also showed the similar CT findings. Light microscopic examination of biopsied biceps brachii (Patient 1) and quadriceps femoris (Patient 2) demonstrated abundant rod-like structures in the majority of type 1 fibers. In both patients, there was a marked variation in fiber size. Type 1 fibers were atrophic and type 2C fibers increased in number.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed2005

Predominantly upper limb weakness, enlarged cisterna magna, and borderline intelligence in a child with de novo mutation of the skeletal muscle alpha-actin gene.

We present a 10-year-old boy from nonconsanguineous parents of Libyan (Sephardi) Jewish origin. Mild dysmorphism, hypotonia, and clubfoot deformities were noted at birth. On follow-up, he had borderline intelligence and nonprogressive muscle weakness, predominantly in the upper extremities. Physical examination revealed mild facial weakness, a bell-shaped chest cavity, kyphosis, winging of the scapula, and hypotonia of the shoulder girdle. Muscle biopsy demonstrated prominent variation in fiber size and central nuclei and numerous subsarcolemmal particles on modified Gomori trichrome stains. Electron microscopy depicted areas of disrupted sarcomeres with abnormal aggregates. Brain magnetic resonance imaging showed mild widening of the lateral ventricles and an enlarged cisterna magna. Molecular DNA analysis by polymerase chain reaction (PCR) and direct sequencing revealed a de novo heterozygous missense mutation in the skeletal muscle alpha-actin gene (ACTA1) changing codon 348 from TCG serine to TTG leucine.

Actins↗

PubMed2001

Increased weakness after pancreas and kidney transplantation.

BACKGROUND: Already there is evidence that simultaneous pancreas and kidney (SPK), or pancreas after kidney (PAK) transplantation, in patients with type 1 diabetes mellitus and end-stage kidney disease prevents worsening of diabetic polyneuropathy, but neuropathic improvement is delayed and incomplete. METHODS: In 85 patients with type 1 diabetes mellitus who underwent SPK or PAK transplantations, we performed sequential neuromuscular evaluations before, every 3 months after, and yearly after transplantation, quantitating muscle weakness separately from overall severity of polyneuropathy. RESULTS: We found that, on average, the weakness subscore of the Neuropathy Impairment Score of the lower limbs [NIS(LL)-W] was significantly worse at 3, 6, 9, and 12 months (by about 5 points) than at baseline. By contrast, for these times after transplantation, a composite score of nerve conduction abnormalities, an independent measure of severity of polyneuropathy, was not significantly worse and, in fact, was significantly improved. In multivariate analysis, length of hospital stay correlated with the increased weakness. CONCLUSIONS: We conclude that: (1) increased neuromuscular impairment after transplantation is mainly due to muscle weakness and not to worsening polyneuropathy; (2) in multivariate analysis, duration of hospitalization after transplantation was significantly associated with this increased weakness; (3) increased weakness is probably due to development of myopathy, which may be related to graft rejection, immunosuppression, sepsis, and intercurrent infections; (4) in future transplantation trials, weakness should be evaluated separately from neuropathic status, and the lowest efficacious dosages of immunotherapy should be used; and (5) essentially all diabetic patients reported that SPK or PAK transplantation was worthwhile because it freed them from diabetic lifestyle concerns.

Adolescent↗

PubMed1992

A clinical, serological, and histopathological study of myositis patients with and without anti-RNP antibodies.

Twenty-nine patients with myositis, including 10 with polymyositis (PM), 6 with dermatomyositis (DM), and 13 with myositis associated with a connective tissue disease (CTD), were followed up for a mean observation time of 49 months. The 13 patients with CTD-associated myositis were further separated by the presence or absence of anti-RNP antibodies. The functional disability at diagnosis was pronounced without differences between the groups. The patients with anti-RNP antibodies did not differ from the other patients regarding initial muscle weakness, erythrocyte sedimentation rate, or creatinine phosphokinase values, but the histopathological muscle changes were generally milder. Rapid improvement of muscle strength on moderate doses of corticosteroids was seen in most patients. At the end of study, corticosteroid treatment had been withdrawn from 17 patients because of remission, including 6 of the 7 patients with anti-RNP antibodies. The presence of electromyographic changes compatible with myositis, pronounced muscle weakness before treatment, and a low erythrocyte sedimentation rate seemed to indicate a less favorable outcome unrelated to diagnostic subgroupings. However, the combination was rarely found among the anti-RNP-positive patients.

Adolescent↗

PubMed2003

Effects of an exercise program on muscle performance in patients undergoing allogeneic bone marrow transplantation.

Allogeneic bone marrow transplantation (BMT) has been successfully used for the treatment of several hematological malignancies; however, it is associated with transplant-related toxicities such as functional impairment and muscle weakness. In order to analyze how an exercise program may influence muscle strength in patients undergoing BMT, we carried out a prospective study assessing patients from the pre-BMT phase to 16 weeks post-BMT. In all, 18 patients underwent three trials: (1) pre-BMT, (2) after marrow engraftment, and (3) 6 weeks after trial 2. After trial 2, the patients were randomized in a control group (CG) or treatment group (TG), which received a 6-week exercise program with active exercise, muscle stretching and treadmill walking. The results obtained in trial 1 showed similar values for CG and TG, as both groups had muscle strength lower than normal patterns based on data concerning age, sex and weight. In trial 2, CG and TG showed similarly decreased values. In trial 3, TG showed values higher than CG for all muscle groups tested. These results suggest that the exercise program was efficient in promoting an increase of muscle strength after allogeneic BMT.

Adolescent↗

PubMed2002

Quantitative analysis of energy metabolism in human muscle using SLOOP 31P-MR-spectroscopy.

OBJECTIVE: Energy metabolism is vital for regular muscle function. In humans, in-vivo analysis using (31)P-MR-spectroscopy (MRS) is mostly restricted to semiquantitative parameters due to technical demands. We applied Spatial Localization with Optimal Pointspread Function (SLOOP) for quantification in human skeletal and cardiac muscle. SUBJECTS/METHODS: 10 healthy volunteers and 4 patients with myotonic dystrophy type 1 were examined using a 1.5 T system (Magnetom VISION) and chemical shift imaging (CSI) for data collection. Concentrations of PCr, ATP and Pi as well as PCr/ATP ratios were calculated by SLOOP. RESULTS: Concentrations of PCr, ATP and Pi were 29.9 +/- 3.4, 7.1 +/- 0.9 and 5.7 +/- 1.2 [mmol/kg] in normal skeletal muscle, corresponding to previously published studies. Two of the patients with a duration of disease longer than 10 years and a pronounced muscle weakness showed a significant decrease of PCr and ATP in skeletal muscle below 10 and 5 mmol/kg. One of these patients had an additional reduction of PCr in cardiac muscle. CONCLUSIONS: With MRS and SLOOP, a more accurate quantitative assessment of metabolism is now available in skeletal and cardiac muscle. Longitudinal studies of larger patient groups will allow to better describe the metabolic disorder in muscle disease over time. Moreover, these techniques offer a new way to quantify treatment effects in future trials.

Adult↗