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PubMed2002

Peak flow and peak cough flow in the evaluation of expiratory muscle weakness and bulbar impairment in patients with neuromuscular disease.

OBJECTIVE: To study the expiratory muscle force and the ability to cough estimated by the peak expiratory flow and peak cough flow in patients with Duchenne muscular dystrophy and amyotrophic lateral sclerosis. DESIGN: A total of 27 patients with amyotrophic lateral sclerosis and 52 patients with Duchenne muscular dystrophy were studied. From the group of 144 normal subjects of this laboratory, we selected 38 for comparison. RESULTS: The maximal inspiratory pressure in patients with Duchenne muscular dystrophy and amyotrophic lateral sclerosis was 64.5 +/- 24.7% and 37.8 +/- 21.8%, respectively, and maximal expiratory pressure was 64.2 +/- 32.5% and 37.7 +/- 21.6%, respectively. Patient groups showed a significant lower peak expiratory flow than normal subjects. Higher peak cough flow than peak expiratory flow was found in all groups. The peak cough flow-peak expiratory flow difference was 46 +/- 18% in normal subjects, 43 +/- 23% in patients with Duchenne muscular dystrophy, and 11 +/- 17% in patients with amyotrophic lateral sclerosis. The peak expiratory flow and peak cough flow were not different in bulbar onset amyotrophic lateral sclerosis. In patient groups, the dynamic and static behavior correlated positively. CONCLUSIONS: These results suggest that peak cough flow-peak expiratory flow is useful to monitor expiratory muscle weakness and bulbar involvement and to assess its evolution in these patients.

Adolescent↗
PubMed1996

Late-onset muscle weakness in partial phosphofructokinase deficiency: a unique myopathy with vacuoles, abnormal mitochondria, and absence of the common exon 5/intron 5 junction point mutation.

Three patients (ages 51, 59, and 79) from two generations of an Ashkenazi Jewish family had partial (33% activity) phosphofructokinase (PFK) deficiency that presented with fixed muscle weakness after the age of 50 years. MR spectroscopy revealed accumulation of phosphomonoesters during exercise. Muscle biopsy showed a vacuolar myopathy with increased autophagic activity and several ragged-red and cytochrome c oxidase-negative fibers. The older patient, age 79 at biopsy, had several necrotic fibers. Electron microscopy revealed subsarcolemmal and intermyofibrillar glycogen accumulation and proliferation of mitochondria with paracrystalline inclusions, probably related to reduced availability of energy due to impaired glycolysis. The common point mutation of exon 5/intron 5 junction seen in Jewish Ashkenazi patients with PFK deficiency was excluded. We conclude that late-onset fixed muscle weakness occurs in partial PFK deficiency and it may represent the end result of continuing episodes of muscle fiber destruction. Partial enzyme deficiency in two successive generations suggests a unique molecular mechanism.

Adult↗
PubMed1997

Respiratory muscle weakness and normal ventilatory drive in dilative cardiomyopathy.

BACKGROUND: In dilative cardiomyopathy several factors influence dyspnoea. Patients with chronic heart failure may demonstrate impairment of breathing pattern, ventilatory drive and respiratory muscle strength, as well as reduction of ventilatory efficiency. The purpose of this study was to evaluate whether dilative cardiomyopathy is accompanied by changes in breathing pattern, respiratory muscle weakness and ventilatory neural drive. METHODS: We investigated 47 patients (36 men, mean age = 47.8 +/- 11.2 years) with chronic heart failure due to dilative cardiomyopathy, and 30 healthy subjects (10 men, mean age = 35.4 +/- 11.7 years) served as controls. Patients and controls underwent evaluation of left ventricular ejection fraction by 2D echocardiography, spirometry, body plethysmography, mouth occlusion pressure and respiratory muscle strength, as well as by submaximal treadmill exercise testing with gas exchange measurements. The patients' results were compared to controls and predicted standard normal values, and evaluated for differences according to the degree of severity of functional impairment. RESULTS: Patients with dilative cardiomyopathy demonstrated a slight reduction in lung volumes (15% of the patients with obstructive and 15% with restrictive lung function pattern) and diffusion capacity (20.4 +/- 6.8 vs 15.4 +/- 6.7 ml.min-1.kPa-1; P < 0.01). In neural drive, as assessed by mouth occlusion pressure, there was no significant difference between patients and controls. There was a slight but significant reduction in respiratory muscle strength, as assessed by measuring maximal inspiratory pressure in patients with dilative cardiomyopathy (6.7 +/- 2.4 kPa vs 8.6 +/- 3.5 kPa; P < 0.01). The observed changes were more pronounced in the severe chronic heart failure patients (with a reduction in ventilatory efficiency) whereas no relationship among indices of cardiac or respiratory function was found. CONCLUSIONS: Patients with chronic heart failure due to dilative cardiomyopathy develop respiratory muscle weakness without changes in neural ventilatory drive, and slight changes in breathing pattern related to the severity of the disease.

Adult↗
PubMed2006

Compensatory strategies during normal walking in response to muscle weakness and increased hip joint stiffness.

Compared to young adults, older adults exhibit a slower walking speed, smaller step length, shorter swing phase time and decreased range of motion in their lower extremity joints. The underlying mechanisms causing these gait adaptations is not well understood, with various musculoskeletal parameters being put forth as contributing factors, including increased joint stiffness and decreased isometric muscle strength. The objective of this study was to identify the necessary compensatory mechanisms to overcome such musculoskeletal deficits and regain a normal walking pattern. Understanding these mechanisms has important implications for designing effective rehabilitation interventions for older adults that target specific muscle groups and properties (e.g., isometric strength versus joint stiffness) to improve gait performance. Muscle-actuated forward dynamics simulations of normal walking were analyzed to quantify compensatory mechanisms in the presence of muscle weakness in specific muscle groups and increased hip joint stiffness. Of particular importance were the compensatory mechanisms provided by the plantar flexors, which were shown to be able to compensate for many musculoskeletal deficits, including diminished muscle strength in the hip and knee flexors and extensors and increased hip joint stiffness. This importance was further highlighted when a normal walking pattern could not be achieved through compensatory action of other muscle groups when the uniarticular and biarticular plantar flexor strength was decreased as a group. Thus, rehabilitation or preventative exercise programs may consider focusing on increasing or maintaining plantar flexor strength, which appears critical to maintaining normal walking mechanics.

Adaptation, Physiological↗
PubMed1990

Respiratory muscle weakness and dyspnea in thyrotoxic patients.

Dyspnea on exertion is a frequently reported symptom of thyrotoxicosis. In the majority of cases, there is no obvious cause of dyspnea, but as skeletal myopathy is also common in thyrotoxic patients, it has been postulated that increased dyspnea could be secondary to respiratory muscle weakness. We sought to determine whether thyrotoxic patients were in fact more dyspneic on exertion than age- and sex-matched controls, and if so, whether the increased dyspnea was secondary to respiratory muscle weakness. The study group consisted of 12 thyrotoxic patients and 12 control subjects matched for age and gender. We measured lung volumes, compliance, elastic recoil, respiratory muscle strength, maximal exercise performance, and the intensity of breathlessness (modified Borg scale) at various levels of exercise in all subjects. The respiratory muscles were weaker in patients than controls. This weakness improved in treated patients (p less than 0.05) with concomitant increases in VC, IC, and TLC (all p less than 0.05). Despite this, we found no differences in breathlessness intensity scores between patients and controls or in patients before and after successful antithyroid therapy.

Adult↗
PubMed1995

Muscle weakness and myalgia. MR imaging investigation.

The status of muscle integrity need no longer be surmised on the basis of gross clinical assessments of muscle strength and invasive procedures. MR imaging brings to the clinical arena new capabilities to aid the management of patients with common muscle complaints of common and uncommon causes. Although findings on MR imaging tend to be nonspecific, muscle structural lesions can be defined in terms of extent and gross composition, and thus help direct invasive procedures and monitor therapies. Radiologists need to remember that their observation of muscle lesions on MR imaging may be the serendipitous discovery of the true cause of a patient's compliant.

Diagnosis, Differential↗
PubMed2001

A suspected case of proximal diabetic neuropathy predominantly presenting with scapulohumeral muscle weakness and deep aching pain.

A 48-year-old man with a 14-year history of type 2 diabetes with proliferative diabetic retinopathy and distal symmetrical diabetic polyneuropathy visited our hospital. Eight months later, he subacutely developed difficulty in both shoulder movement and trouble standing up from a squatting position. This was accompanied by severe bilateral shoulder and thigh pain. Magnetic resonance imaging of the brain, cervical and lumbar spine, computed tomography of the shoulder and X-ray films of the cervical spine and shoulder revealed no abnormality. Cerebrospinal fluid showed a mild elevation of protein (0.93 g/l) without cell infiltration. Antiganglioside antibodies and point mutation of mitochondrial DNA at position 3243 were not found. Neuropathology of the sural nerve showed a moderate myelinated fiber loss, active axonal degeneration, but onion-bulb formation, endoneurial or epineurial vasculitis were not observed. Electromyography revealed neurogenic changes in the proximal upper limb muscles. Nerve conduction studies revealed mild bilateral slowing in nerve conduction velocity in both of the upper and lower limbs. The diagnosis of this patients was suspected to be a proximal diabetic neuropathy (diabetic amyotrophy). The pain and muscle weakness had persisted more severely in the shoulder than in the thigh throughout the clinical course. His unbearable symptoms could be partially alleviated by an administration of a selective serotonin reuptake inhibitor, fluvoxamine maleate. Proximal diabetic neuropathy is a rare disabling type of neuropathy, which is characterized with subacute bilateral muscle weakness and wasting in the proximal part of the lower limbs. The involvement of the scapulohumeral region observed in this case is very unusual in proximal diabetic neuropathy.

Anorexia↗
PubMed2001

Magnesium deficiency promotes muscle weakness, contributing to the risk of sudden infant death (SIDS) in infants sleeping prone.

A review was published (1991) of 19 retrospective case-control studies that had investigated the relationship between prone sleeping position (on the stomach) and the sudden infant death syndrome (SIDS). These studies, which had been conducted between 1965 and 1990 in New Zealand, Australia, England, France and the Netherlands, showed an overall higher rate of SIDS in infants who usually slept prone. In those countries, vigorous community intervention to change babies' sleep position away from the prone has resulted in marked declines of 50 per cent or more in the rate of SIDS. Such encouraging reports from many countries prompted the American Academy of Pediatrics to recommend that infants be placed to sleep on their backs to reduce the risk of SIDS. This was followed by a successful campaign in the United States between mid-1994 and 1998. Despite the decreased incidence, SIDS remains the leading cause of death in infants 1 month to 1 year of age of industrialized nations of the world. Studies have been conducted in human infants, mechanical models and animal models to learn the role of risk factors in prone sleeping infants. Soft bedding, thermal stress and biologic risk factors such as impaired ventilatory and arousal responsiveness are among many factors that have been investigated. Hunt states that there is not a single unifying factor that explains increased SIDS in prone sleeping infants. Two major studies conducted in the 1970s showed: (1) muscle weakness in the upper half of the body in infants who subsequently died of SIDS, and (2) shoulder hypotonia in near-miss for SIDS infants. An infant sleeping face-down in the prone position could be jeopardized if he lacked the muscle strength to shift his position or turn his head to rescue himself from a life-threatening situation. In contrast, recent studies in neonates sleeping in the prone position report that normal infants can spontaneously arouse and turn their heads. Some data support the hypothesis that magnesium deficiency contributes to SIDS. Muscle strength is seriously impaired in the young magnesium deficient subject, while magnesium rapidly reverses muscle weakness. In rats, marginal deprivation in dietary magnesium reduces exercise capacity, an early effect of magnesium deficiency which is preventable by consuming magnesium-enriched mineral water. It is concluded that magnesium deficiency is at least one major unifying factor that explains increased SIDS in prone sleeping infants.

Humans↗
PubMed2004

Morphometric characterization of the neuromuscular junction of rodents intoxicated with 2,4-dithiobiuret: evidence that nerve terminal recycling processes contribute to muscle weakness.

2,4-Dithiobiuret (DTB) causes ascending motor weakness when given chronically to rodents. In muscles of animals with DTB-induced weakness, quantal release of acetylcholine (ACh) is impaired. We examined in detail the structural changes that occurred at neuromuscular junctions and their associated Schwann cells of extensor digitorum longus (EDL) muscles of male rats treated with DTB to the onset of muscle weakness, 5-8 days. Our objective was to assess the involvement of the Schwann cells and to determine the most likely primary targets of DTB. At the onset of muscle weakness, nerve terminals exhibited some enlarged regions, but did not sprout. Terminal Schwann cells became flatter and expanded to cover most of the endplate. The extent of invasion of the synaptic cleft by Schwann cell processes was not significantly different from controls; extension of Schwann cell sprouts away from the junction was not seen. Thus, the morphology of the Schwann cells, although clearly affected by DTB, does not suggest that they contribute directly to the physiological defects of DTB-treated terminals. Abnormal tubulovesicular structures or tangles of neurofilaments were clustered in the centers of about 25% of treated terminals. Fewer synaptic vesicles occupied the region opposite the postsynaptic folds. Vesicle volumes were variable and included some very large vesicles, corresponding with the variable MEPP amplitudes reported previously for terminals of DTB-treated rodents. The postsynaptic area stained by rhodamine-labeled alpha-bungarotoxin expanded with terminal swelling, apparently by unpleating of the postsynaptic folds. No loss of ACh receptors or spread of ACh receptors beyond terminal boundaries was detected. Morphometric data are consistent with the conclusion that DTB affects, either directly or indirectly, vesicular release of ACh and the subsequent vesicular recycling process.

Animals↗
PubMed1987

Skeletal muscle weakness resulting from quinidine ingestion.

We have described a patient with muscle weakness caused by ingestion of quinidine sulfate. Intrafascicular perivasculitis and rare muscle fiber regeneration were present in the muscle at biopsy. A similar clinical picture has previously been reported in patients taking other medications, but not quinidine.

Aged↗
PubMed1996

Acetylcholine receptor epsilon-subunit deletion causes muscle weakness and atrophy in juvenile and adult mice.

In mammalian muscle a postnatal switch in functional properties of neuromuscular transmission occurs when miniature end plate currents become shorter and the conductance and Ca2+ permeability of end plate channels increases. These changes are due to replacement during early neonatal development of the gamma-subunit of the fetal acetylcholine receptor (AChR) by the epsilon-subunit. The long-term functional consequences of this switch for neuromuscular transmission and motor behavior of the animal remained elusive. We report that deletion of the epsilon-subunit gene caused in homozygous mutant mice the persistence of gamma-subunit gene expression in juvenile and adult animals. Neuromuscular transmission in these animals is based on fetal type AChRs present in the end plate at reduced density. Impaired neuromuscular transmission, progressive muscle weakness, and atrophy caused premature death 2 to 3 months after birth. The results demonstrate that postnatal incorporation into the end plate of epsilon-subunit containing AChRs is essential for normal development of skeletal muscle.

Animals↗
PubMed1998

New laryngeal muscle weakness in post-polio syndrome.

The authors describe the clinical presentations of post-polio laryngeal muscle weakness in three patients with prior polio infection who presented with new complaints including slowly progressive dyspnea, dysphagia, and/or hoarseness. Evaluations by laryngeal videostroboscopy and electromyography revealed vocal cord abductor and/or adductor weakness, recurrent posterior glottic web in one case, and, in the two patients who agreed to electromyography, evidence of prior denervation and reinnervation in laryngeal muscles. Treatment was directed at attempting to maintain an airway and optimize vocal quality. One patient benefitted from tracheostomy, one benefitted from vocal cord medialization, and one benefitted from resection of interarytenoid scarring. The authors conclude that diagnosis of laryngeal post-polio syndrome is facilitated by laryngeal electromyography. Interventions directed at maintaining an appropriate airway and optimizing vocal quality may be helpful.

Aged↗
PubMed1994

[Autopsy case of amyloidosis with marked cardiac and pulmonary lesions associated with myeloma, initially presenting with muscle weakness].

A 69-year-old man presented initially with muscle weakness of the bilateral lower limbs. Chest roentgenogram showed diffuse reticulonodular shadows, bilateral hilar lymphadenopathy, and dullness of bilateral costophrenic angles. Chest CT showed thickening and irregularity of vascular shadows, and thickening of bronchial walls. On the first admission we could not diagnose pulmonary or muscle lesions. He was subsequently admitted for the deterioration of congestive heart failure, but there was no improvement. Myocardial biopsy demonstrated deposition of amyloid in the cardiac muscular tissue. Autopsy revealed amyloid deposition in pulmonary vasculature, alveolar septal walls and pleura. Amyloid deposition was also recognized systemically in skeletal muscles, lymph nodes, liver, kidney, spleen, stomach, and intestines. We recognized about 20% IgA lambda-positive plasma cells with atypia, and myeloma-associated amyloidosis diagnosed. This case was classified as diffuse alveolar septal form and pleural form of pulmonary amyloidosis. We could find only a few reports of pleural form, which exhibits an interesting distribution.

Aged↗
PubMed1983

An unusual cause of hypokalemic muscle weakness.

A 36-year-old woman presented with proximal muscle weakness, cramps, and a serum potassium level of 2.7 mEq/l. During her hospitalization she was noted to use excessive quantities of a snuff preparation containing glycyrrhizinic acid, a potent mineralocorticoid analogue. With discontinuation of this substance, her potassium returned to normal values and her strength improved. This case is submitted as a hypokalemia myopathy induced by snuff dipping.

Adult↗
PubMed1993

Effect of diazepam on muscle weakness in a model of myasthenia gravis in rats.

Rats chronically received alpha-bungarotoxin which caused a reduction of nicotinic acetylcholine receptors and weakness, especially of lip muscles. It was found that diazepam (0.75-2 mg kg-1, s.c.), after a 15 min period of excitation and increased lip weakness, caused sedation and some improvement of the lip. Even after 5 mg kg-1 diazepam, muscle function was not markedly affected and breathing appeared normal. It is concluded that sedation in rats by diazepam does not entail aggravation of the muscle weakness caused by a partial neuromuscular block.

Animals↗
PubMed2004

Severe respiratory muscle weakness related to long-term colchicine therapy.

We report a case of colchicine-induced myopathy, in which the initial presenting and predominant clinical feature was respiratory muscle dysfunction; there was also chronic renal failure and electromyographically-measured myopathy. Discontinuation of colchicine led to marked improvement. Colchicine discontinuation was the only therapy performed (other medications were unchanged), and within 3 weeks the patient had regained motor function and resumed daily activities. Myopathy from primary biliary cirrhosis was ruled out. In contrast to acute colchicine intoxication, chronic colchicine toxicity is related to prolonged use rather than colchicine serum level, so colchicine serum level was not measured and did not affect the decision to discontinue colchicine. Although the diagnosis was not confirmed by muscle biopsy, we believe the typical presentation and the rapid improvement after withdrawing colchicine confirm the diagnosis. We conclude that long-term colchicine therapy, especially in the setting of chronic renal failure, can produce symptomatic respiratory muscle weakness.

Colchicine↗
PubMed2001

Low score normal muscle weakness alters cardiac decorin expression: implication for cardiac collagen fibril organization.

Cardiac decorin and Type I collagen expression and collagen fibrosis were examined in a chicken line exhibiting the low score normal (LSN) genetic muscle weakness and compared to normal cardiac muscle at 14 and 20 d of embryonic development and at 1 and 6 wk posthatch. These extracellular matrix proteins were selected due to their role in regulating tissue elasticity, which is critical for normal cardiac function. Beginning at 1 wk posthatch, relative levels of decorin were higher in the LSN cardiac muscle than in the control, indicating a time-dependent increase in decorin expression. Type I collagen levels appeared to be unaffected by the LSN condition. Morphologically, myocardial and coronary artery fibrosis did not differ between the control and LSN at all stages examined. These results are suggestive of extracellular matrix remodeling in LSN cardiac muscle that is mediated through a decorin-dependent pathway.

Animals↗