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PubMed2005

[Falls in peripheral neuropathy].

Falling accidents are predisposing factors in worsening the quality of life. Causes of falls included gait and balance problems, visual disorder, cognitive impairment and drugs. However, falls in neuropathic patients are not often investigated. We studied the actual condition and causes of falls associated with neuropathy. One hundred and ninety-three patients (122 males and 71 females, ages 57 +/- 15 years) with neuropathy were selected for evaluation. In all patients, more than half a year had passed since the onset of symptoms and the present condition was considered comparatively stable. We divided the patients into 2 groups: falling or non-falling. Patients experiencing accident accompanied by external injury once or more in the past year, or patients who answered "often fell" (1 time or more per month) on flat ground or in their residence comprised the fall group. The severity of disease was evaluated by modified Rankin Scale (0 to 5). The relationship between falls and neuropathic symptoms (proximal muscle weakness, distal muscle weakness, aching or numbness, and the position and vibration sensory loss) was statistically examined. The distribution of patients in the fall group according to modified Rankin Scale of neuropathy was scale 5: 0/0 (0%), scale 4: 5/36 (14%), scale 3: 24/72 (33%), scale 2: 7/56 (13%), and scale 1: 1/19 (5%). There were six fractures among all patients. Regarding the etiology, the fall group showed a high level of axonal neuropathies (44%). On analysis according to condition and symptoms in the patients with a score of 2, 3, or 4 who demonstrated a high rate of falls, there was a strong correlation between deep sensory loss and fall (p < 0.05). However, as independent factors, there were no correlations between falling and proximal muscle weakness, distal muscle weakness or aching numbness, respectively. We thought it necessary to add ataxic gait resulting from deep sensory loss to one of the fall risks.

Accidental Falls↗
PubMed2002

Weakness of respiratory and skeletal muscles after a short course of steroids in patients with acute lung rejection.

There have been occasional reports of acute respiratory and skeletal muscle weakness in intensive care unit patients treated with massive doses of corticosteroids. However, in this setting the concomitant use of other drugs may have influenced the finding. In this study the effects of 5 days of treatment with high doses of steroids in consecutive patients with acute lung rejection after transplantation were systematically evaluated. Maximal inspiratory pressure during phrenic nerve stimulation and peak torque of isokinetic contraction of the quadriceps and hamstring muscles were measured objectively. Compared to the pretreatment condition, approximately 45% of patients showed acute generalised muscle weakness that recovered after approximately 2 months. This demonstrates muscle weakness induced by steroids within patients.

Adrenal Cortex Hormones↗
PubMed1999

Respiratory muscle involvement in multiple sclerosis.

Respiratory complications are common in the terminal stages of multiple sclerosis and contribute to mortality in these patients. When respiratory motor pathways are involved, respiratory muscle weakness frequently occurs. Although it is well established that weakness of the respiratory muscles produces a restrictive ventilatory defect, the degree of muscle weakness and pulmonary function are poorly related. Respiratory muscle weakness was observed in patients with normal or near normal pulmonary function. Expiratory muscle weakness is more prominent than inspiratory muscle weakness and may impair performance of coughing. Subsequently, in addition to bulbar dysfunction, respiratory muscle weakness may contribute to ineffective coughing, pneumonia, and sometimes even acute ventilatory failure may ensue. Respiratory muscle weakness may also occur early in the course of the disease. Recent studies suggest that the respiratory muscles can be trained for both strength and endurance in multiple sclerosis patients. Whether respiratory muscle training delays the development of respiratory dysfunction and subsequently improves exercise capacity and cough efficacy, prevents pulmonary complications or prolongs survival in the long-term remains to be determined.

Humans↗
PubMed2005

Treatment of malabsorption vitamin D deficiency myopathy with intramuscular vitamin D.

A nearly 5 year-old boy presented with proximal muscle weakness, reduced muscle bulk, a positive Gower sign and Trendelenburg gait. He was known to have cholestatic liver disease. Investigations revealed markedly low serum total calcium, elevated alkaline phosphatase, very low serum 25-hydroxyvitamin D, and radiographs consistent with active rickets despite the ongoing administration of a water-soluble preparation of vitamin D. Only i.v. calcitriol acutely corrected the hypocalcemia, despite trying several oral preparations, suggesting that malabsorption secondary to chronic liver disease was the cause of his rickets. Intramuscular calciferol quickly corrected his muscle weakness and X-ray findings. Myopathy secondary to vitamin D deficiency is an uncommon diagnosis in children. Intermittent calciferol is an inexpensive and practical treatment for vitamin D deficiency, especially if associated with malabsorption.

Child, Preschool↗
PubMed2004

Spontaneously remitting dermatomyositis.

Dermatomyositis (DM) is an inflammatory myopathy of skeletal muscle with characteristic cutaneous findings. It is a rare disorder with a bimodal age distribution that affects almost twice as many women as men. One category of DM, normal-enzyme DM, is characterized by cutaneous changes only at baseline, normal serum muscle enzyme levels and myositis demonstrated by electromyography (EMG) and/or muscle biopsy specimens. Typically, patients with normal-enzyme DM progress to severe muscle involvement and require systemic corticosteroid therapy. The patient we report has normal-enzyme DM confirmed by serial serum enzymes, EMG, and skin and muscle biopsies but is unique in that she never experienced progression of muscle weakness although muscle involvement was documented histologically and by EMG. Follow-up examination after 1 year revealed near-complete resolution of cutaneous involvement after topical therapy and no evidence of muscle weakness.

Aged↗
PubMed1998

Lack of effect of oral Mg-supplementation on Mg in serum, blood cells, and calf muscle.

UNLABELLED: Magnesium (Mg) is important for regulating ion transport and cellular metabolism in all body tissues. In skeletal muscle Mg is involved in the neuromuscular activity, excitation, and muscle contraction. Mg deficiency can cause muscle weakness and muscle cramps. Less than 1% of total body Mg is found in serum, yet the serum Mg concentration is used to assess the body's Mg status. PURPOSE: The purpose of this study was to determine whether an oral Mg supplementation (500 mg Mg-oxide.d-1 for 3 wk) affects exercise performance, clinical symptoms, and the Mg concentration in various body compartments in athletes with low-normal serum Mg levels (N = 10 in each group). METHODS: In a double-blind, placebo-controlled study, correlation analysis between the Mg concentration in serum, blood cells, and skeletal muscle was performed to establish a measure for muscle cell Mg. RESULTS: The data indicate that a 3-wk Mg supplementation did not affect exercise performance, neuromuscular activity, or muscle related symptoms. Also, the supplementation did not increase the Mg concentration in serum or any cellular compartment studied. However, in the placebo group the renal Mg clearance decreased, whereas it increased in the subjects receiving Mg supplementation. Correlation analysis revealed that serum Mg only correlated with red cell Mg and that only leukocyte Mg correlated with the nuclear magnetic resonance (NMR)-measured muscle cell Mg concentration. CONCLUSIONS: These results indicate that Mg supplementation in athletes with low-normal serum Mg did not improve performance and failed to increase the body's Mg stores. Serum Mg appears to be a poor indicator for Mg in skeletal muscle or most other cellular compartments, but the concentration of Mg in mononuclear leukocytes might be used as an indicator of skeletal muscle Mg when NMR is not available.

Administration, Oral↗
PubMed2006

Pulmonary rehabilitation in patients with neuromuscular disease.

In neuromuscular disease (NMD) patients with progressive muscle weakness, respiratory muscles are also affected and hypercapnia can increase gradually as the disease progresses. The fundamental respiratory problems NMD patients experience are decreased alveolar ventilation and coughing ability. For these reasons, it is necessary to precisely evaluate pulmonary function to provide the proper inspiratory and expiratory muscle aids in order to maintain adequate respiratory function. As inspiratory muscle weakening progresses, NMD patients experience hypoventilation. At this point, respiratory support by mechanical ventilator should be initiated to relieve respiratory distress symptoms. Patients with adequate bulbar muscle strength and cognitive function who use a non-invasive ventilation aid, via a mouthpiece or a nasal mask, may have their hypercapnia and associated symptoms resolved. For a proper cough assist, it is necessary to provide additional insufflation to patients with inspiratory muscle weakness before using abdominal thrust. Another effective method for managing airway secretions is a device that performs mechanical insufflation-exsufflation. In conclusion, application of non-invasive respiratory aids, taking into consideration characterization of respiratory pathophysiology, have made it possible to maintain a better quality of life in addition to prolonging the life span of patients with NMD.

Breathing Exercises↗
PubMed1977

Weakness in myotonic syndromes.

Muscle weakness occurs in a number of myotonic syndromes, including those in which muscle bulk is preserved. The possible causes of muscle weakness may be considered in terms of the different stages of the electromechanical activation process and defects in the contractile machinery. In individual myotonic disorders the ability to identify the origin of the muscle weakness (whether neurogenic or myogenic) and the functional level at which the defect occurs would assist the choice of rational treatment.

Action Potentials↗
PubMed1987

Abnormal ventilatory chemosensitivity and congenital myopathy.

Abnormal ventilatory function is common in patients with neuromuscular disorders. This report describes depressed ventilatory response to both hypoxia and hypercapnia, as well as arterial oxygen desaturation during sleep in a family with congenital myopathy. The index patient also had an abnormal ventilatory response to metabolic acid loading. There was clinical evidence of proximal muscle weakness, and a muscle biopsy specimen was consistent with myopathy. The reduction in ventilatory drive, however, could not be explained solely by ventilatory muscle weakness. This report describes a distinct familial syndrome of congenital myopathy and abnormal ventilatory response to hypercapnia and hypoxia. All affected family members had unique facial features, proximal muscle weakness, and impaired ventilatory responses. The combination of impaired ventilatory drive and reduced ventilatory muscle strength leaves patients particularly vulnerable, and heightened awareness of this association is important in the treatment of these patients.

Adult↗
PubMed2000

Functional motor unit failure precedes neuromuscular degeneration in canine motor neuron disease.

Hereditary canine spinal muscular atrophy (HCSMA) features rapidly progressive muscle weakness that affects muscles in an apparent proximal-to-distal gradient. In the medial gastrocnemius (MG) muscle of homozygous HCSMA animals, motor unit tetanic failure is apparent before the appearance of muscle weakness and appears to be presynaptic in origin. We determined whether structural changes in neuromuscular junctions or muscle fibers were apparent at times when tetanic failure is prevalent. We were surprised to observe that, at ages when motor unit tetanic failure is common, the structure of neuromuscular junctions and the appearance of muscle fibers in the MG muscle were indistinguishable from those of symptom-free animals. In contrast, in more proximal muscles, many neuromuscular junctions were disassembled, with some postsynaptic specializations only partially occupied by motor nerve terminals, and muscle fiber atrophy and degeneration were also apparent. These observations suggest that the motor unit tetanic failure observed in the MG muscle in homozygous animals is not due to synaptic degeneration or to pathological processes that affect muscle fibers directly. Together with previous physiological analyses, our results suggest that motor unit failure is due to failure of neuromuscular synaptic transmission that precedes nerve or muscle degeneration.

Animals↗
PubMed1993

Respiratory muscles and ventilatory failure: 1993 perspective.

Some conditions that predispose to ventilatory failure increase the work of breathing (chronic obstructive pulmonary disease [COPD], obesity, kyphoscoliosis), whereas others cause severe respiratory muscle weakness. Specific reasons for muscle weakness include critical illness (electrolyte imbalance, acidemia, shock, sepsis), chronic illness (poor nutrition, cachexia), and neuromuscular diseases. Inspiratory muscle weakness from mechanical disadvantage to the diaphragm is characteristic of asthma and COPD. The increased work of breathing combined with muscle weakness increases the pressure needed to inspire a breath and decreases maximal inspiratory pressure. When this pressure exceeds 0.4, dyspnea and inspiratory muscle fatigue ensue. One way to lower this pressure and avert fatigue is to lower the tidal volume. Ventilatory drive is high, not low, in ventilatory failure. Concomitant shortening of inspiration and breath duration cause the small tidal volume and increased respiratory rate. Gas exchange is compromised by ventilation/perfusion imbalance, and the ratio of dead space to tidal volume is also increased by rapid, shallow breathing. Reduction in tidal volume minimizes dyspnea, but the small tidal volume is inadequate for gas exchange. Acute treatment of respiratory muscle failure involves respiratory muscle rest through mechanical ventilation and removal of noxious influences (infection, metabolic disarray), whereas chronic treatment involves rebuilding the contractile apparatus by nutritional repletion and training.

Animals↗
PubMed1979

Central core disease: clinical and pathological evidence of progression within a family.

A family is described whose members showed different clinical presentations of central core disease. In 4 members the myopathy was congenital and nonprogressive, but in 2, muscle weakness first developed in adult life. Two further members had raised CPK levels without muscle weakness. Muscle weakness in one of the late-onset cases increased over eighteen months. This was associated with evidence of loss of type 2 fibres and the appearance of type 3 fibres on muscle biopsy. It is suggested that central core disease involves reinnervation of type 2 fibres by type 1 axons, and that the clinical manifestation of the disease depends on the age of onset and rate of progression of this process.

Adolescent↗
PubMedDate not supplied

Clinical forms of acquired myasthenia gravis in dogs: 25 cases (1988-1995).

The purpose of this project was to investigate the clinical forms of acquired myasthenia gravis in dogs. The medical records from 25 dogs with seropositive acquired myasthenia gravis were reviewed, and the following data were recorded for each patient: signalment, history, clinical findings; results of IV edrophonium chloride administration, repetitive nerve stimulation, and presence or absence of muscle membrane staining by immunocytochemical methods; serum acetylcholine receptor antibody concentration; treatment; and outcome. Several clinical forms of acquired myasthenia gravis were identified. Nine of the 25 patients (36%) had no historical or clinical evidence of appendicular muscle weakness, and were designated as focal myasthenics. These dogs exhibited focal weakness in one or more of the following muscle groups: facial (3 of 9), pharyngeal (3 of 9), and laryngeal (3 of 9). The remaining 16 dogs (64%) exhibited appendicular muscle weakness. Four of these 16 dogs had acute onset and rapid development of clinical signs, and were designated as acute fulminating myasthenics. The remaining 12 dogs were classified as generalized myasthenics. All 4 dogs with acute fulminating myasthenia gravis had megaesophagus, 2 had facial muscle weakness, and 1 had pharyngeal muscle weakness. Ten of the 12 dogs with generalized myasthenia gravis had megaesophagus, 4 had facial muscle weakness, 4 had pharyngeal muscle weakness, and 3 had laryngeal muscle weakness. Historical or clinical evidence of exercise-associated appendicular weakness was found in only 6 of the 12 (50%) dogs with generalized myasthenia gravis, and in none of the dogs with acute fulminating myasthenia gravis. Seven of the 12 dogs with generalized myasthenia gravis had weakness primarily (n = 1) or exclusively (n = 6) of the pelvic limbs. Two of the 4 dogs with acute fulminating myasthenia gravis had primarily pelvic limb weakness. Twelve of the 25 dogs (48%) died or were euthanized shortly after admission to the hospital due to aspiration pneumonia. The dogs with acute fulminating myasthenia gravis had a markedly higher 1-year mortality rate in comparison with the other 2 groups. The use of immunosuppressive therapy had a significant positive effect on patient survival, regardless of the type of myasthenia gravis. This investigation demonstrates that acquired myasthenia gravis in dogs is a disorder with a wide spectrum of clinical forms, similar to the analogous disorder in people.

Animals↗
PubMedDate not supplied

Which is more useful, the "full can test" or the "empty can test," in detecting the torn supraspinatus tendon?

The purpose of this study was to determine the clinical usefulness of the full can and empty can tests for determining the presence of a torn supraspinatus tendon. The two tests were performed in 143 shoulders of 136 consecutive patients. In each test, the muscle strength was determined by manual muscle testing, and the presence of pain during the maneuver was recorded. We interpreted the tests as positive when there was 1) pain, 2) muscle weakness, or 3) pain or muscle weakness or both. Shoulders were examined by high-resolution magnetic resonance imaging with 95% accuracy for full-thickness rotator cuff tears. There were 35 shoulders with full-thickness tears of the supraspinatus tendon. The accuracy of the tests was the greatest when muscle weakness was interpreted as indicating a torn supraspinatus tendon in both the full can test (75% accurate) and the empty can test (70% accurate). However, there was no significant difference between the accuracy of the tests when this criterion was used. Pain was observed in 62 shoulders (43%) during the full can test and in 71 shoulders (50%) during the empty can test, but the difference was not statistically significant. Muscle weakness should be interpreted as indicative of supraspinatus tendon tear. Using this indicator, both tests are equivalent in terms of accuracy, but considering pain provocation, the full can test may be more beneficial in the clinical setting.

Adolescent↗