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PubMed1985

Adult-onset muscle weakness. How to identify the underlying cause.

When adults present with muscle weakness as the predominant symptom and sign, the causes can usually be narrowed down to four disorders: amyotrophic lateral sclerosis, Guillain-Barré syndrome, myasthenia gravis, and inflammatory myopathy. Perhaps the most difficult task for the clinician is identifying which of these patients are actually weak and which are describing generalized fatigue. This task should be made easier by keeping in mind the definition of muscle weakness--a loss of power resulting in reduction of motor function--and by performing careful functional muscle testing.

Adult↗
PubMed1963

LIGHT AND ELECTRON MICROSCOPIC STUDIES OF "MYOGRANULES" IN A CHILD WITH HYPOTONIA AND MUSCLE WEAKNESS.

Examination by light and electron microscopy of more than 100 muscle biopsies revealed one very unusual case. A 4-year-old boy with non-progressive muscle weakness and hypotonia was found to have small particles, termed "myogranules", in many muscle fibres from two gastrocnemius biopsies. Paraffin sections and thin sections of plastic-embedded muscle showed that the rod-shaped myogranules measured between 0.1 and 5 microns in length, and were usually orientated in the long axis of the fibre. Normal cross-striations could not be seen in areas occupied by myogranules, although adjacent parts of the same fibre were normal. Electron micrographs showed myofilaments running through the myogranules and a periodicity similar to sections of recrystallized muscle protein paramyosin. It is possible that this child has a disturbance of muscle proteins.

Actin Cytoskeleton↗
PubMed2002

Difference in distribution of muscle weakness between myasthenia gravis and the Lambert-Eaton myasthenic syndrome.

BACKGROUND: Myasthenia gravis and the Lambert-Eaton myasthenic syndrome (LEMS) may have a similar distribution of muscle weakness. Deciding on a diagnosis of myasthenia gravis or LEMS on clinical grounds may therefore be difficult. OBJECTIVE: To compare the localisation of initial muscle weakness and the distribution of weakness at the time of maximum severity in patients with myasthenia gravis and LEMS. SUBJECTS: 101 patients with myasthenia gravis and 38 patients with LEMS. RESULTS: In myasthenia gravis, initial weakness involved extraocular muscles in 59%, bulbar muscles in 29%, and limb muscles in 12% of the patients. In LEMS no patient had ocular weakness, 5% had bulbar weakness, and 95% had weakness of the limbs as the first symptom (p < 0.001). At the point of maximum severity, weakness in myasthenia gravis was purely ocular in 25%, oculobulbar in 5%, restricted to the limbs in 2%, and present in both oculobulbar muscles and limbs in 68%. At this point, none of the LEMS patients had weakness restricted to extraocular or bulbar muscles (p = 0.002). The legs were affected in all LEMS patients, whereas in 12 patients with generalised myasthenia gravis limb weakness was restricted to the arms (p = 0.024). CONCLUSIONS: In a patient suspected to have a myasthenic syndrome whose first symptom is ocular weakness, LEMS is virtually excluded. Limb weakness confined to the arms is only found in generalised myasthenia gravis and not in LEMS. Muscle weakness in myasthenia gravis tends to develop in a craniocaudal direction, and in the opposite direction in LEMS.

Adolescent↗
PubMed2006

Paroxysmal muscle weakness: the familial periodic paralyses.

The familial periodic paralyses (PP) were commonly considered to be benign diseases since frequency and severity of the paralytic attacks decrease in adulthood. However, with increasing age, a third of the patients develop permanent weakness and muscle degeneration with fatty replacement. Another complication, cardiac arrhythmia, can result from the dyskalemia during paralytic attacks. The familial PP are typical dominant ion channelopathies: the function of the mutant muscular channel is compensated in the interictal state but defective under certain conditions which then cause flaccid weakness. A triggering factor is the level of serum potassium, the extracellular ion decisive for membrane excitability. In hyper- and hypokalemic periodic paralysis, the mutations are specifically located in the voltage-gated sodium and calcium channels which are essential for action potential generation or excitation-contraction coupling. The common mechanism for the membrane inexcitability during paralytic attacks is a transient membrane depolarization that inactivates the sodium channels which are then no longer available for action potential generation. For the third PP type, the Andersen syndrome, the responsible gene is also expressed in cardiac muscle, and, independently of paralytic attacks, the hazard of ventricular arrhythmias is inherent. The gene product, an inwardly rectifying potassium channel, is responsible for maintaining the resting membrane potential, and all known mutations cause dominant-negative effects on the tetrameric channel complexes. In this article the clinical consequences of the mutations and the therapeutic strategies for all three types of PP are reported.

Humans↗
PubMed2006

Inspiratory muscle training in patients with heart failure and inspiratory muscle weakness: a randomized trial.

OBJECTIVES: This study sought to evaluate the effects of inspiratory muscle training in inspiratory muscle strength, as well as in functional capacity, ventilatory responses to exercise, recovery oxygen uptake kinetics, and quality of life in patients with chronic heart failure (CHF) and inspiratory muscle weakness. BACKGROUND: Patients with CHF may have reduced strength and endurance in inspiratory muscles, which may contribute to exercise intolerance and is associated with a poor prognosis. METHODS: Thirty-two patients with CHF and weakness of inspiratory muscles (maximal inspiratory pressure [Pi(max)] <70% of predicted) were randomly assigned to a 12-week program of inspiratory muscle training (IMT, 16 patients) or to a placebo-inspiratory muscle training (P-IMT, 16 patients). The following measures were obtained before and after the program: Pi(max) at rest and 10 min after maximal exercise; peak oxygen uptake, circulatory power, ventilatory oscillations, and oxygen kinetics during early recovery (VO2/t-slope); 6-min walk test; and quality of life scores. RESULTS: The IMT resulted in a 115% increment Pi(max), 17% increase in peak oxygen uptake, and 19% increase in the 6-min walk distance. Likewise, circulatory power increased and ventilatory oscillations were reduced. The VO2/t-slope was improved during the recovery period, and quality of life scores improved. CONCLUSIONS: In patients with CHF and inspiratory muscle weakness, IMT results in marked improvement in inspiratory muscle strength, as well as improvement in functional capacity, ventilatory response to exercise, recovery oxygen uptake kinetics, and quality of life.

Breathing Exercises↗
PubMedDate not supplied

Symptoms in patients with primary hyperparathyroidism: muscle weakness or sleepiness.

OBJECTIVE: To evaluate the effects of parathyroidectomy on the nonspecific symptoms associated with primary hyperparathyroidism, with an emphasis on distinguishing sleepiness from muscle weakness. METHODS: We conducted a prospective cohort study of consecutive patients presenting for parathyroidectomy for the treatment of primary hyperparathyroidism. Twenty-three patients underwent assessment preoperatively and postoperatively. The Functional Outcomes of Sleep Questionnaire (FOSQ), the Epworth Sleepiness Scale (ESS), and a questionnaire of disease-specific symptoms were administered preoperatively, 2 weeks postoperatively, and 4 to 6 months postoperatively. The FOSQ assesses how sleepiness alters daytime performance, and the ESS reflects the degree of daytime sleepiness. RESULTS: All 23 patients achieved normocalcemia postoperatively. Although no significant changes were found in the overall scores for the FOSQ and ESS after parathyroidectomy, there was a significant decline in the overall mean incidence of disease-specific symptoms postoperatively (P <or=0.0001 after 2 weeks and P = 0.0020 after 4 to 6 months). The five disease-specific symptoms that significantly decreased in frequency postoperatively were (1) muscle weakness, (2) polydipsia, (3) dry skin and itching, (4) memory loss, and (5) anxiety. CONCLUSION: In this study, patients with primary hyperparathyroidism did not demonstrate daytime sleepiness or difficulty performing everyday activities because of sleepiness at baseline or after successful parathyroidectomy. The overall mean percentage for incidence of disease-specific symptoms, however, significantly declined postoperatively, especially in reference to muscle weakness.

Aged↗
PubMed1980

Proximal muscle weakness in uremia. Case reports and review of the literature.

Weakness of the proximal muscle groups developed in six uremic patients, five men and one woman, while receiving hemodialysis. All showed roentgenographic evidence of renal osteodystrophy. Partial to complete recovery of strength followed subtotal parathyroidectomy in four patients. All patients had normal levels of creatine phosphokinase. Electrodiagnostic testing showed features of both "myopathic" and denervating processes on coaxial needle exploration and normal to slowed nerve conduction. Muscle biopsy specimens in four patients showed type 2 fiber atrophy with no evidence of necrosis, phagocytosis, regeneration, or vasculitis. The pathogenesis of proximal muscle weakness in uremia is uncertain but may be related to secondary hyperparathyroidism or osteodystrophy.

Adult↗
PubMed2003

Muscle weakness in critically ill children.

OBJECTIVE: To establish the incidence of muscle weakness in critically ill children. METHODS: Neuromuscular examinations were performed in 830 children without identified antecedent or acute neuromuscular disease (age 3 months to 17 years 11 months) admitted for >24 hours to a pediatric intensive care unit (ICU) over a 1-year period. RESULTS: Fourteen of 830 (1.7%) patients had generalized weakness. Four failed repeated attempts to extubate. Multiple organ dysfunction occurred in 11 patients and sepsis in 9. Most children received corticosteroids, neuromuscular blocking agents, or aminoglycoside antibiotics. Eight of the 14 children were solid organ or bone marrow transplant recipients. Muscle biopsy showed evidence of acute quadriplegic myopathy in all three patients in whom biopsy was performed. Three patients died. In survivors, significant weakness persisted for 3 to 12 months following ICU discharge. CONCLUSIONS: Muscle weakness is an infrequent but significant feature of critical illness in children. Transplant recipients seem to be at particular risk.

Adolescent↗
PubMed1986

Chronic renal failure presenting as proximal muscle weakness in a child.

A 13-year old boy presented with a three-year history of slowly progressive proximal muscle weakness, particularly involving the lower extremities. Chronic renal failure was uncovered in the course of his evaluation. Urologic investigation showed small and poorly functioning kidneys with a BUN of 118 mg/dL and a creatinine of 10.7 mg/dL. There were no anomalies of the proximal or distal collecting systems or history suggestive of recurrent urinary tract infection. The neurologic examination revealed proximal muscle weakness primarily of the lower extremities and especially of the proximal musculature of the pelvic girdle. Nerve conduction studies were normal. The electromyogram (EMG) showed high-voltage polyphasic potentials consistent with neurogenic muscle disease. A biopsy of the right quadriceps muscle demonstrated type II muscle fiber atrophy with histochemical staining. The patient's clinical findings, EMG studies, and muscle biopsy were not specific for either neurogenic or myopathic disease. Following a period of home peritoneal dialysis and renal transplantation, there was significant clinical improvement of the muscle weakness.

Adolescent↗
PubMed2000

Skeletal muscle weakness is associated with wasting of extremity fat-free mass but not with airflow obstruction in patients with chronic obstructive pulmonary disease.

BACKGROUND: Skeletal muscle weakness is a prominent problem in many patients with chronic obstructive pulmonary disease (COPD). OBJECTIVE: The aim of the study was to determine the relation between skeletal muscle function, body composition, and lung function in COPD (emphysema and chronic bronchitis) patients and healthy volunteers. DESIGN: In 50 patients with chronic bronchitis, 49 patients with emphysema, and 28 healthy volunteers, skeletal muscle function was assessed by handgrip and linear isokinetic dynamometry. Whole-body and subregional fat-free mass (FFM) were assessed by dual-energy X-ray absorptiometry. RESULTS: Whole-body and extremity FFM were significantly lower in patients with emphysema (P < 0.001) and chronic bronchitis (P < 0.05) than in healthy volunteers, but trunk FFM was significantly lower only in patients with emphysema (P < 0.001). Extremity FFM was not significantly different between the COPD subtype groups, despite significantly lower values for whole-body and trunk FFM (P < 0.05) in patients with emphysema. Absolute skeletal muscle function (P < 0. 001) and muscle function per kilogram of whole-body FFM were significantly lower in both COPD subtype groups than in healthy volunteers (P < 0.05), but no significant difference was found between patients with chronic bronchitis and those with emphysema. Muscle function per kilogram of extremity FFM was not significantly different between the 3 groups and was not associated with forced expiratory volume in 1 s. CONCLUSION: Skeletal muscle weakness is associated with wasting of extremity FFM in COPD patients, independent of airflow obstruction and COPD subtype.

Absorptiometry, Photon↗
PubMed2026

Validation and refinement of a biomarker panel for frailty assessment and prediction of muscle weakness in older adults.

Frailty is a complex geriatric syndrome characterized by age-related declines in physiological function and cognitive reserve. To promote early prevention and intervention, minimally invasive and objective biomarkers that can detect frailty progression are required. We aimed to identify biomarkers associated with frailty progression and to elucidate their relevance to the Japanese version of the Cardiovascular Health Study (J-CHS) criteria, consist of five components (unintentional weight loss, self-reported exhaustion, muscle weakness, slow walking speed, and low physical activity). A total of 168 individuals (61 robust, 25 pre-frail, and 82 frail) enrolled in the NCGG (National Center for Geriatrics and Gerontology) Biobank were analyzed. Clinical information, blood-test data, aging-related factors, and gene-expression data were integrated for the analysis. First, linear regression identified one clinical factor, five aging-related factors, and 251 gene-expression factors associated with frailty. Subsequent logistic regression analyses examining each J-CHS components highlighted six candidate biomarkers. Cross-validation further suggested that three of these biomarkers-SMI, apelin, and GDF15-may represent potential biomarkers. Finally, retrospective and prospective analyses further demonstrated that those biomarkers were predictive of future muscle weakness, yielding a concordance index of 0.70. In conclusion, we validated and refined a biomarker panel consisting of SMI, apelin, and GDF15 that is associated with frailty, particularly muscle weakness (a major J-CHS component). These biomarkers may be useful for frailty assessment. Longitudinal analyses further suggested that they may be associated with the future development of muscle weakness in initially robust older adults, although validation in larger prospective cohorts is warranted.

Journal Article↗
PubMed2001

[Prolonged muscle weakness associated with the administration of non-depolarizing neuromuscular blocking agents in critically ill patients].

Generalized muscle weakness is a common disorder in patients undergoing mechanical ventilation. The cause is unknown but is attributed to the administration of non-depolarizing neuromuscular blocking and other drugs, mainly steroids, or to the presence of sepsis or multiorgan failure. Specific clinical pictures (polyneuropathy, myopathy and prolonged muscle weakness) develop in function of the underlying cause, although etiological factors may sometimes interact. Differential diagnosis is carried out with the aid of electromyography and pathology of the peripheral muscle. Costs are high and prognosis is uncertain. Completeness of neuromuscular blockade must be monitored in these patients to guide the administration of drugs, to avoid overdoses, to maintain muscle activity and to detect a chain of reactions among concomitant medications or pathophysiologic changes.

Critical Illness↗
PubMed1997

[Prolonged muscle weakness in intensive care patients with special attention to the so-called intensive care polyneuromyopathy].

Generalized muscle weakness in critically ill patients can result in prolonged periods of artificial ventilation and longer stays in the intensive care unit. Both neuropathic (critical illness polyneuropathy) and myopathic (critical illness myopathy) abnormalities seem to play an important role for this prolonged weakness. This article reviews its complex differential diagnosis with special emphasis on the current understanding of the neuromuscular syndromes. An efficient diagnostic plan is necessary for the exclusion of other curable causes of prolonged muscle weakness even in the presence of polyneuromyopathic changes. Psychological support of the patient and prophylaxis of secondary complications of prolonged immobilization are crucial when specific therapy is not possible.

Critical Care↗
PubMedDate not supplied

Muscle weakness in infants with rickets: distribution, course, and recovery.

We describe the distribution, progression, and resolution of muscle weakness, wasting, and hypotonia in three infants with rickets due to different causes. Progressive muscle weakness affecting preferentially the proximal muscles of the legs and failure to gain weight were the presenting symptoms. The skeletal signs appeared later in the course of the illness and the time for resolution of the neuromuscular findings varied with the etiology of the disorder.

Calcium Gluconate↗
PubMed2000

[A family with oculopharyngeal muscular dystrophy with (GCG)9 expansion in which a sister had neck as well as proximal and her brother proximal lower limb muscle weakness].

We report a 58-year-old woman (patient 1) and her 60-year-old brother (patient 2) with autosomal dominant oculopharyngeal muscular dystrophy. Patient 1 first noticed blepharoptosis and neck weakness at age 55. On neurological examination, she showed bilateral blepharoptosis and weakness in the neck and upper proximal limbs. Serum creatine kinase (CK) level was slightly elevated. Her older brother first noticed blepharoptosis and lower limb weakness at age 51. On neurological examination, he showed bilateral blepharoptosis, slight ophthalmoparesis and bilateral iliopsoas muscle weakness. Serum CK level was normal. Esophageal fluoroscopy disclosed dysfunction of the constrictor pharyngeal muscles. Muscle biopsy of them showed myopathic changes with rimmed vacuoles. The (GCG)9 mutation in the poly (A) binding protein 2 gene was identified, which was the same as seen in the large French-Canadian kindred in Quebec in Canada. The clinical phenotype in patient 2 is similar to that of French-Canadian patients but it in patient 1 is different in distribution of muscle weakness.

DNA-Binding Proteins↗
PubMed1984

Effect of respiratory muscle weakness on P0.1 induced by partial curarization.

Mouth occlusion pressure 0.1 s after onset of inspiration (P0.1) reflects central respiratory drive (CRD), but its dependence on respiratory muscle strength is unknown. To clarify this relationship, we produced progressive levels of respiratory muscle weakness by infusion of d-tubocurarine in eight supine spontaneously breathing normal subjects. Hypercapnic ventilatory response (HCVR) was measured before curarization and at mild (mean inspiratory effort 62 +/- 3% of control), moderate (42 +/- 3%), and severe (23 +/- 1%) weakness. At the severe level of weakness 1) supine functional residual capacity was not significantly changed from base line, 2) the percent of base-line slope of delta P0.1/delta PCO2 (122 +/- 27%) was significantly greater (P less than 0.01) than that for change in expired minute ventilation (delta VE)/delta PCO2 (39 +/- 10%), 3) the percent of base-line delta P0.1/delta VE (381 +/- 46%) during HCVR was significantly increased (P less than 0.01), 4) the P0.1 response was significantly increased from base line at two out of three specific levels of PCO2 while the VE was unchanged or significantly decreased, and 5) peak inspiratory resistance did not significantly change. Thus P0.1, unlike VE, did not decrease with even severe respiratory muscle weakness. Indeed, P0.1 increased at two out of three levels of PCO2 under circumstances when higher CRD is expected. One potential explanation for the results is that P0.1 may at least qualitatively reflect CRD up to the level of severe respiratory muscle weakness attained in this study.

Adult↗
PubMed1996

[A case of a thoracic extradural arachnoid cyst presenting with slowly progressive muscle weakness in the right upper and lower limbs].

A 49-year-old woman developed slowly progressive muscle weakness of the right upper and lower limbs. Physical examination revealed exaggeration of deep tendon reflexes in bilateral lower extremities and a Th5-Th6 girdle sensation. Weakness in her right upper extremity suggested cervical or intracranial lesion. Neuroradiological studies detected no abnormalities in her cervical cord and cranium. So the symptoms and signs were similar to those of motor neuron disease except for the sensory disturbance. MRI study of thoracic cord demonstrated a thoracic extradural arachnoid cyst. After removal of the cyst, the patient's muscle weakness was prominently relieved. We postulate that the cyst stretched spinal cord and dura mater, which led to affection of her cervical cord. We propose weakness of an upper limb as a pseudo-localizing sign of a thoracic extradural arachnoid cyst.

Arachnoid Cysts↗