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PubMed2002

Inhibition of maximal voluntary contraction force by experimental muscle pain: a centrally mediated mechanism.

Muscle weakness frequently accompanies conditions with musculoskeletal pain. It is not clear if this attenuation of force is due to peripheral or central processes. The effect of experimental muscle pain on maximal voluntary contraction torque and peripheral contractile properties was therefore assessed. Experimental muscle pain reduced the torque produced by isometric knee extension, but the contractile properties assessed by twitch interpolation were not affected. This indicates that force inhibition by muscle pain is centrally mediated. This has clinical implications for rehabilitation and training of patients with musculoskeletal pain.

Adult↗

PubMed2005

The uremic environment and muscle dysfunction in man and rat.

BACKGROUND: Patients reaching end-stage renal disease experience debilitating fatigue, with progression of this disease, rendering patients dysfunctional in their everyday lives. METHODS: In vivo measurements of muscle function, assessed using surface electromyography (EMG), were made on 25 patients prior to and after a session of hemodialysis (HD) treatment, along side in vitro measurements of muscle function in isolated rat muscles incubated in normal or uremic conditions approximating to those found in uremic rats (rat uremic: RU) or uremic humans (human uremic: HU). RESULTS: HD significantly affected plasma values, e.g. reducing urea (69%), creatinine (62%), potassium (23%) and phosphate (48%) concentrations in patients (all p < 0.01). Treatment also improved the EMG frequency of 2nd dorsal interosseous (fast-twitch) (p < 0.01), although no change was noted for vastus lateralis (slow-twitch). In isolated rat muscles, a uremic environment had no significant effect on slow-twitch soleus during field stimulation, however, in fast-twitch extensor digitorum longus, a significant 23% (RU) and 22% (HU) faster rate of decline in force was measured, compared to controls (p < 0.001 and p < 0.01, respectively). CONCLUSION: It is concluded that (1) muscle weakness and its electrophysiological correlates may be rapidly induced by uremic solutes and rapidly reversed when the solutes are removed by dialysis, and (2) fast-twitch muscles are more readily affected by uremic conditions than slow-twitch muscles.

Adult↗

PubMed2001

[A thyrotoxic myopathy accompanied with unusual muscle symptoms and MRI muscle findings].

We report a patient with thyrotoxic myopathy associated with unusual muscle symptoms. A 29-year-old man developed hyperhidrosis, diarrhea, increase in appetite, and excitability in July, 1999. In August, he experienced muscle stiffness in bilateral lower extremities after maintaining postures such as driving a car or sitting on a chair. He was admitted to our hospital, in January, 2000. On physical examination, goiter was noted. Neurological examination was normal except for proximal muscle weakness. Laboratory test showed elevated free T3 and free T4, decreased TSH. TSH receptor antibody was increased. MRI of lower extremities revealed atrophy of bilateral biceps femoris. Muscle strength increased gradually after an oral administration of thiamazole 30 mg/day, and muscle stiffness disappeared. The clinical features of this patient and differential diagnosis were discussed.

Adult↗

PubMed1991

[A case of delayed myeloneuropathy due to malathion intoxication].

We report a patient with serious organophosphorus-induced delayed neurotoxicity due to malathion. The patient was a 49-year-old male with a history of habitual alcohol drinking, who ingested approximately 100 ml of 50% malathion [S-1,2-bis(ethoxycarbonyl)-ethyl-0,0-dimethyl phosphorodithioate solution], with a large amount of alcohol in a suicide attempt. Following recovery from an acute cholinergic phase 36 hours after ingestion, respiratory muscle weakness, consciousness disturbance and diffuse weakness of the limb muscles occurred, necessitating mechanical ventilation. On the 7th hospital day, glove and stocking type sensory disturbance was observed and weakness of the limbs had progressed to distal dominant flaccid quadriparalysis with moderate muscle atrophy. Two months after onset, neurogenic bladder and spinal automatism became obvious. After 7 months, spasticity of the lower limbs developed, while the weakness of the upper limbs improved. Sural nerve biopsy showed axonal degeneration, loss of large myelinated fibers and increases in Schwann cell clusters. These findings were similar to those seen in patient with triorthocresyl phosphate (TOCP) intoxication. The symptoms of this patient seemed to correspond to Senanayake's "intermediate syndrome". The final clinical features and sural nerve biopsy findings were in close agreement with those in patients with serious organophosphorus compounds induced delayed neurotoxicity due to TOCP intoxication. However, this patient exhibited more severe neuropathy than seen in previously reported cases of organophosphorus compounds induced delayed neurotoxicity caused by less toxic organophosphorus compounds, such as Dipterex. This suggests that alcohol might have been an etiological factor in damage of nervous tissue in this rare case. This is the first case of organophosphorus compounds induced delayed neurotoxicity due to malathion to be reported in Japan.

Biopsy↗

PubMed1982

Respiratory mechanics in supine subjects during progressive partial curarization.

Respiratory mechanics were studied in six supine conscious volunteers during progressive muscle weakness produced by infusion of d-tubocurarine. Partial curarization was carried out to the point of abolishing head lift ability and handgrip strength. At all levels of partial paralysis, expiratory muscle strength was significantly more impaired than inspiratory strength. Despite this, subjects maintained relatively normal maximal expiratory flow rates, whereas inspiratory flows decreased significantly. The diminished inspiratory flows are not fully explained by decreased driving pressures during force inspiration, since inspiratory resistance increased significantly with the decreased flow. Inspiratory flow patterns suggest a variable extrathoracic obstruction most likely due to the absence of normal airway abductor activity during inspiration. Maximal respiratory muscle weakness decreased forced vital capacity by 29% and total lung capacity by 15%. The decreased level of lung inflation did not alter lung elastic recoil. Functional residual capacity was unchanged, but inspiratory capacity decreased by 25% and residual volume increased by 38%. These changes are in accord with predictions based on the decreased muscle strength and normal respiratory system recoil.

Adult↗

PubMed2003

Brief assessment of motor function: reliability and concurrent validity of the Gross Motor Scale.

OBJECTIVE: The Brief Assessment of Motor Function (BAMF) is a series of 10-point ordinal scales developed for rapid description of gross motor, fine motor, and oral motor performance. We examined interrater and intrarater reliability and concurrent validity of the BAMF Gross Motor Scale. DESIGN: This validation study included 48 children (age, 5 mo to 17 yr) with a wide range of gross motor capability. Ten children with varied diagnoses participated in the reliability study. For concurrent validity, the BAMF performance of 38 children with osteogenesis imperfecta was compared with scores on the Peabody Developmental Motor Scales, laboratory gait analysis, and manual muscle testing. RESULTS: Reliability values for intraclass correlations were 0.996 (interrater) and 1.00 (intrarater). Significant relationships were identified between the BAMF and gait speed ( r = 0.68, P < 0.0001), stride length (r = 0.71, P < 0.0001), duration of double-limb support ( r = -0.40, P < 0.03), number of weak muscles (r = -0.74, P< 0.0001), and the Peabody Developmental Motor Scales (r = 0.95, P < 0.0001). Number of weak muscles was the strongest predictor of BAMF score R2 = 0.5080, F = 24.77, P < 0.0001). CONCLUSIONS: The BAMF demonstrates good reliability for children with a range of diagnoses and acceptable concurrent validity with gross motor development, muscle strength, and formal gait assessment in children with osteogenesis imperfecta.

Activities of Daily Living↗

PubMed1999

Changing views about 'Osteoporoses' (a 1998 overview).

Recent realizations have begun to change how 'osteoporoses' are diagnosed, managed and studied. This article explains the nature and basis of some resulting controversies, chiefly for clinicians who manage such patients but do not participate in resolving those controversies. Currently the size of a bone 'mass' deficit serves to diagnose 'osteoporosis', but recently clarified physiology suggests at least three different kinds of osteoporosis could occur in people with identical bone 'mass' deficits. Indeed, they do occur. (a) In one kind, people have less bone than 'normal' but no bone problems unless they sustain injuries. Most of their resulting fractures, usually from falls, affect extremity bones. This condition can affect children, men and women. (b) In a second kind an osteopenia exists in which voluntary physical activities (not injuries) cause spontaneous fractures and/or bone pain, mainly in the spine, more often in women than men and seldom in children (osteogenesis imperfecta excepted). (c) A third kind combines features of the first two. As for the physiology involved in those affections, bone modeling can increase bone strength and 'mass', while BMU (Bone Multicellular Unit)-based bone remodeling can reduce them. Mainly bone strains control those two activities and muscles cause the largest strains, so muscle strength should strongly influence bone modeling, remodeling, strength and 'mass'. If so chronic muscle weakness should usually cause an osteopenia and weakened bones. Excessive amounts of fatigue damage or microdamage can also weaken bones. From that physiology one could argue that chiefly chronic muscle weakness instead of an intrinsic bone disorder would cause (a), while intrinsic but still enigmatic modeling and remodeling disorders would cause (b), and (c) could combine features of both conditions. If so, these ideas could have significant effects on the future criteria used to diagnose osteoporoses and osteopenias, on how they are studied in the clinic and laboratory, and on how they are prevented or, if they occur, are managed.

Adolescent↗

PubMed1987

Clinical correlations of antibodies that bind, block, or modulate human acetylcholine receptors in myasthenia gravis.

Acetylcholine receptor (AChR) binding and AChR modulating antibodies were found with approximately the same frequency (86%) in 349 patients with myasthenia gravis (MG). However, the total yield of positive serological results was significantly improved (90%) by assaying AChR modulating antibodies when AChR binding antibodies were not detected, because in 27 patients (8%) only one of the two tests was positive. The immunoprecipitation test for AChR blocking antibodies yielded fewer positive results (52%), but there was a significant correlation between the degree of AChR blockade and generalization of muscle weakness. In no patient was this the only positive test, because the test for AChR modulating antibodies in this study detected both AChR blocking and modulating antibodies. Human muscle AChR was used as antigen in all tests. False positive results were rare and were attributed to unexplained antibodies to 125I-alpha-Bgt (AChR binding antibody assay) and recent general anesthesia using muscle relaxants (AChR blocking and AChR modulating antibody assays). Unexplained positive results, documented previously in 5% of patients with the Lambert-Eaton myasthenic syndrome and amyotrophic lateral sclerosis (ALS), were found in this study in two of 22 patients with ALS, but in none of 427 patients with miscellaneous neurological diseases. Patients with severe generalized MG and/or thymoma tended to have higher titers of AChR binding antibodies and greater AChR modulating antibody activity. However, some patients with severe muscle weakness had low titers of antibodies, and some patients in remission or with only ocular manifestations had high titers. These seemingly paradoxical results reflect heterogeneity in the specificities, affinities, and isotypes of anti-AChR antibodies. To effect pathogenicity, antibodies must have access in vivo to extracellular antigenic sites on the AChR. One would anticipate that antibodies with greatest pathophysiological potential would be of an IgG with greatest pathophysiological potential would be of an IgG subclass that activates complement, or of a specificity that competes for acetylcholine's binding site on the receptor or readily cross-links two AChR molecules to trigger receptor modulation (e.g., by binding to sites on the duplicated alpha-subunit). In patients with suspected MG who lack serological evidence of anti-AChR antibodies, motor endplate biopsy is required for microelectrophysiological, immunochemical, and ultrastructural studies to establish with certainty whether or not the condition is acquired MG.

Autoantibodies↗

PubMed1991

[A case of adult T cell leukemia/lymphoma with motor and sensory polyneuropathy].

A 62-year-old man was admitted to our hospital because of two months continuing paresthesia and muscle weakness of distal portions of the four limbs. On general physical examination, skin lesions, lymphadenopathy and hepatosplenomegaly were not found. Neurological examination revealed moderate weakness in the bilateral distal muscles of the lower limbs and left distal muscles of the upper limbs, and slight weakness in the right distal muscles of the upper limbs and the bilateral proximal muscles of the four limbs. Hand grasping powers were 24 kg and 2 kg on the right and left, respectively. The biceps, triceps and radial reflexes were decreased on the right, but normal on the left. The Achilles tendon reflex was decreased on the right and absent on the left. Paresthesia and superficial sensory disturbance were observed with glove and stocking distribution, which was more severe on the left side. The vibration and position senses were slightly decreased in the distal part of the lower limbs. On the laboratory examinations, serum anti-HTLV-I antibody was positive and no abnormal lymphocytes were observed in peripheral blood. Cerebrospinal fluid findings were normal, and anti-HTLV-I antibody was negative. Motor and sensory conduction velocities were normal or slightly decreased in all of the limb nerves examined, but the amplitudes of the compound muscle action potentials and the sensory nerve action potentials were asymmetrically decreased. Needle EMG showed fibrillation potentials and giant spikes with a reduction in number of motor unit potentials. The histological examination of the biopsied sural nerve revealed severe axonal degeneration without evidence of vasculitis or infiltration of abnormal lymphocytes.(ABSTRACT TRUNCATED AT 250 WORDS)

CD4-CD8 Ratio↗

PubMedDate not supplied

Balance, muscle strength, and fear of falling in older adults.

This study examined balance ability, lower-extremity muscle strength, fear of falling and their inter-relationships in 40 community-dwelling older adults (>65 years). Subjects who self-identified either as being fearful of falling or not (no concern) were screened to exclude those with known risk factors for falling. Limits of stability, maximal isometric strength, gait speed, and fear of falling were contrasted between groups (27 control subjects, 13 fearful subjects). Those fearful of falling demonstrated smaller center of pressure (COP) excursions in anterior, left, and right directions (p<.0001) and used a smaller percentage of their base of support during maximal weight shifting in combined anterior-posterior and right-left directions (p<.001) compared to the control group. Strength did not differ between groups, but was associated with the ability to shift the COP in the anterior-posterior direction (p<.05). Fear of falling also related to weight shifting ability (p<.017). Seniors fearful of falling demonstrated limitations in balance ability and balance confidence that could not be explained by muscle weakness.

Aged↗

PubMed1992

Respiratory function in multiple sclerosis. Utility of clinical assessment of respiratory muscle function.

PURPOSE: The aim of this study was to assess the utility of clinical assessment of respiratory muscle weakness in MS. PATIENTS AND METHODS: We studied 40 MS patients who performed pulmonary function tests using standard procedures and measures of respiratory muscle strength. Descriptive clinical indices included a history of detailed neurologic findings, including upper and lower extremity weakness, cerebellar signs, and evidence of cerebral lesions and other clinical signs including dependence in activities of daily living, shortness of breath, weak voice, dysarthria and dysphagia. We devised an index comprised of four clinical signs: the patient's report of difficulty in clearing pulmonary secretions and his report of a weakened cough, the examiner's observation of the patient's cough, and ability to count on a single exhalation. RESULTS: Mean values of TLC (95 percent +/- 14) VC (91 percent +/- 19), and RV (106 percent +/- 34) were normal. By contrast, MVV (68 percent +/- 20), PImax (74 percent +/- 27) and PEmax (51 percent +/- 22) were decreased. Stepwise multiple regression indicated that the best single predictor of expiratory muscle weakness was the index score; the combination of index score, upper extremity weakness, and maximal voluntary ventilation accounted for 60 percent of the variance in PEmax. CONCLUSION: We conclude that clinical assessment is a better predictor of respiratory muscle weakness than spirometry and that a systematic clinical assessment supplemented by respiratory muscle assessment and MVV can uncover subtle respiratory muscle weakness in patients with MS.

Adult↗

PubMed1992

Glycogen storage disease type III with muscle involvement: reappraisal of phenotypic variability and prognosis.

A review of the case histories of 19 Japanese patients with enzymatically proven glycogen storage disease (GSD) III who developed muscular symptoms at various ages illustrates the phenotypic variability of this disease. There seem to be 4 subgroups of GSD III with muscle involvement according to the clinical symptoms. The first group of patients is characterized by the childhood onset of muscle weakness and hepatic disorders. The second group of patients develops muscular symptoms in adult years while the liver symptoms start in childhood. The third group includes the patients whose muscle weakness started in adult years long after liver symptoms in childhood had disappeared. The fourth group shows only muscular symptoms as adults without any sign or history of liver dysfunction since childhood. The prognosis for each subgroup seems to be different; however, none of them appears to be better than that for GSD I, as has been suggested previously.

Female↗

PubMed1980

Treatment of hypophosphataemic vitamin D-resistant rickets and adult presenting hypophosphataemic vitamin D-resistant osteomalacia.

The results of the treatment of 12 patients with hypophosphataemic vitamin D-resistant rickets, 4 similar patients who were first diagnosed in adulthood, and 2 adult patients with hypophosphataemic vitamin D-resistant osteomalacia are presented. Treatment with a high dosage of Vitamin D2 was begun between 1 1/2 and 7 years of age. The dose of Vitamin D2 required for the treatment of rickets varied widely depending on the severity of the process and the age of the patient. Four patients with leg deformities required osteotomy or other operations. In other patients deformities improved with medical treatment alone. Dwarfism and severe deformity of the legs were characteristic features in rickets first diagnosed in adulthood. Radiographic features were Looser's zones, a coarse trabecular pattern, increased bone density and ligamentous calcification. These patients presented several difficult orthopaedic problems. Two brothers with hypophosphataemic vitamin D-resistant osteomalacia presented with bone pains, muscle weakness, limitation of motion in the back and height loss. Treatment with oral phosphate supplements in addition to high doses of Vitamin D2 was dramatic, with complete disappearance of muscle weakness and bone pain.

Adolescent↗

PubMedDate not supplied

Does balance control deficit account for walking difficulty in Parkinson's disease?

Patients with Parkinson's disease (PD) walk slowly, in part to compensate for their balance control deficit. We tested the effect of balance support to determine if walking performance in PD patients would improve. The sample consisted of unmedicated older adults with idiopathic Parkinson's disease who had poor balance control but no stooped posture, arthritis or muscle weakness. There was no difference in walking speed between unsupported and supported walking. The speeds were between those reported for disease-free older adults and older adults with muscle weakness and a history of falling. PD patients' walking difficulties, even while using a balance aid, may be partly explained by their set-changing problems. They frequently hold the cane off the ground when walking, suggesting their set-changing difficulty may be severe enough that using it aggravates their walking difficulty. Treatment of walking difficulty in PD patients should consider interventions other than those dealing only with balance control.

Adult↗

PubMed1998

[Clinical and pathological studies on nemaline myopathy in adulthood].

We examined 22 biopsied muscles from adult patients who had the histopathological characteristics of nemaline myopathy. In the first group, 13 patients had muscle weakness and/or skeletal abnormalities, such as high-arched palate, pes cavus and scoliosis which are often accompanied with the congenital nemaline myopathy. Their appropriate diagnosis had never been made until muscle biopsy was done, because of benign clinical course. In the second group, the symptoms of nine patients became manifest in adulthood and failed to show typical skeletal abnormalities. However, six muscle biopsies showed the histopathologic characteristics of congenital nemaline myopathy; abnormal fiber type distribution including type 1 fiber predominancy, type 1 fiber atrophy and type 2B fiber deficiency. Three patients remained in good health until adulthood when they developed muscle weakness with pathologic findings of nemaline myopathy. Accordingly, nemaline myopathy in adulthood can be categorized into three forms; the first two forms have clinical and pathologic evidence of the congenital benign form, whereas the symptoms are too mild to be noticed. The third form is not a hereditary disorder which may result from autoimmune pathophysiology.

Adolescent↗

PubMed1991

Respiratory muscle strength and control of ventilation in patients with neuromuscular disease.

To assess the relationship between respiratory mechanics and muscle strength and control of ventilation in patients with neuromuscular disease (NMD), we compared PImax and PEmax at RV, FRC and TLC, total respiratory elastance (Ers) with VT, TI, TT, VE, VT/TI, TI/TT, P.01, and P.01/(VT/TI) effective impedance in 21 patients with NMD and 21 healthy control (C) subjects, in seated position breathing room air. Ers in NMD patients was 79 percent higher than in the C subjects. While TI, TT, and VT in NMD were approximately half the corresponding C values, P.01 was 66 percent greater than in the C subjects (both p less than 0.001). NMD PImax and PEmax ranged from 37 to 52 percent of corresponding C values, respectively. Despite significant respiratory muscle weakness, only 7 of 16 patients demonstrated a PaCo2 greater than 45 mm Hg. Ventilatory output in NMD was modulated by respiratory mechanics as indicated by the increased P.01. In spite of muscle weakness, central drive in patients with NMD is not decreased, and in fact, is often increased. VE is not an accurate measure of central drive because of abnormal intrinsic respiratory mechanics and the effects of conscious responses or reflexes.

Adolescent↗

PubMed2005

The natural course of non-classic Pompe's disease; a review of 225 published cases.

Pompe's disease is a neuromuscular disorder caused by deficiency of lysosomal acid alpha-glucosidase. Recombinant human alpha- glucosidase is under evaluation as therapeutic drug. In light of this development we studied the natural course of cases not fitting the definition of classic infantile Pompe's disease. Our review of 109 reports including 225 cases shows a continuous spectrum of phenotypes. The onset of symptoms ranged from 0 to 71 years. Based on the available literature, no criteria to delineate clinical sub-types could be established.A common denominator of these cases is that first symptoms were related to or caused by muscle weakness. In general, patients with a later onset of symptoms seemed to have a better prognosis. Respiratory failure was the most frequent cause of death. CK, LDH, ASAT, ALAT and muscle glycogen levels were frequently but not always elevated. In most cases a muscle biopsy revealed lysosomal pathology, but normal muscle morphology does not exclude Pompe's disease. In 10% of the cases in which the enzyme assay on leukocytes was used, a normal alpha-glucosidase activity was reported. Data on skeletal muscle strength and function, pulmonary function, disability, handicap and quality of life were insufficiently reported in the literature. Studies of non-classic Pompe's disease should focus on these aspects, before enzyme replacement therapy becomes generally available.

Age Distribution↗

PubMedDate not supplied

Acute ethanol treatment decreases intracellular calcium-ion transients in mouse single skeletal muscle fibres in vitro.

Alcohol misuse frequently leads to muscle weakness, which may also occur in the setting of acute and chronic alcoholic myopathies. At the cellular level, ethanol has been found to interfere with signalling mechanisms in cardiac myocytes, skeletal myotubes, and smooth muscle cells. In this study, we focused on the effects of ethanol on the intracellular calcium ([Ca(2+)](i)) transients responsible for excitation-contraction (EC) coupling in isolated mouse skeletal fibres loaded with the fluorescent Ca(2+) indicator fura-2. Following electrical stimulation, ethanol caused a significant reversible dose-dependent reduction in [Ca(2+)](i) transient amplitude, already significant at 100 mM ethanol (P = 0.03), without modifying resting [Ca(2+)](i). Evaluating the potential loci for the effects of ethanol, we indirectly measured sarcolemmal Ca(2+) entry by monitoring Mn(2+)-quenching of intracellular fura-2 via the nitrendipine-sensitive Ca(2+) channels during electrical pacing. Ethanol at doses of 20 mM and greater caused a dose-dependent reduction in the rate of fura-2 quenching (all at P<0.05). Moreover, the intracellular pool of Ca(2+) releasable by caffeine was found to be reduced at a minimum of 300 mM ethanol (P = 0.05). We conclude that ethanol reduces the [Ca(2+)](i) transients underlying EC coupling in single mouse skeletal muscle fibres. This acute effect of ethanol was primarily due to an inhibitory effect of ethanol on sarcolemmal Ca(2+) influx via voltage-operated Ca(2+)-channels and, to a lesser extent, to a reduction in the Ca(2+) sarcoplasmic reticulum loading state. This inhibitory effect of ethanol may be implicated in the development of muscle weakness with alcohol consumption.

Animals↗