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PubMed1985

Adaptive response to ocular muscle weakness in human pursuit and saccadic eye movements.

Eye movement deficits caused by ocular muscle weakness vary according to the position of the eye in the orbit and the direction of eye movement. We studied the ability of both the saccadic and pursuit eye-movement systems to compensate for these anisotropic deficits in four patients with ocular muscle weakness. The eye-position dependence of each patient's motor deficit was characterized by plotting the position of the weak eye against that of the normal eye (in various orbital positions) when fusion was prevented, thus giving a static eye-position curve from which relative muscle strength could be inferred. Movements of the weak eye were smaller and slower than those made by the normal eye, so that the weak eye required more time to acquire a visual target. When patients were forced to view monocularly with their weak eye for several days, both the saccadic and pursuit systems showed changes in the movements of the normal eye consistent with an increased central innervation designed to decrease the time it takes to bring the target's image onto the fovea of the weak eye and to keep it there. These adaptive changes varied with eye position and movement direction and compensated for the weak muscle in both its agonistic and antagonistic actions. Saccadic adaptation consisted of a change in the relationship between saccadic amplitude and retinal error (distance between the target's image and the fovea) to compensate for hypometria (undershoot) and a readjustment of the ratio of the phasic (pulse) and tonic (step) components of the saccadic innervation to suppress postsaccadic ocular drift. Pursuit adaptation consisted of an increase in the relationship between eye acceleration and the rate of motion of the image of the target on the retina during the initial phase of tracking as well as an increase in the velocity during tracking of a target moving at a constant velocity. These changes reflect an increase in pursuit innervation that would cause the weak eye's velocity to approach target velocity sooner. The average acceleration of the normal eye during the initial period of tracking (130 ms) increased by as much as threefold. The corresponding maximum smooth eye velocity increased so that, for example, the pursuit response to a 15 degree/s target movement could be over 50 degree/s in the normal eye.

Adaptation, Physiological↗

PubMed1991

Breathing during sleep in patients with myotonic dystrophy and non-myotonic respiratory muscle weakness.

Sleep apnoea and hypopnoea have been reported in myotonic dystrophy, but it is unclear whether this is simply attributable to the respiratory muscle weakness which is common in this condition. We therefore investigated whether breathing and oxygenation during sleep were more abnormal in patients with myotonic dystrophy than in patients with non-myotonic muscle weakness. Seven subjects were studied in each of three groups: normal controls, myotonic dystrophy and non-myotonic weakness. Patients in the latter group were chosen to represent a similar range of severity of respiratory muscle weakness to those with myotonic dystrophy. Detailed polysomnography was performed; the severity of breathing disorders during sleep was quantified in terms of the frequencies of apnoea and hypopnoea and the degree of arterial desaturation. The myotonic patients showed more frequent apnoea and hypopnoea and more severe desaturation than the other two groups; the results in the non-myotonic patients were generally intermediate. The results suggest that abnormal breathing during sleep is common in myotonic dystrophy and is not due solely to the direct effects of respiratory muscle weakness. Somnolence, which is a well recognized symptom of myotonic dystrophy, was not clearly attributable to the sleep apnoea/hypopnoea syndrome nor to abnormal sleep architecture in the myotonic patients.

Adult↗

PubMed1980

Analysis of lung volume restriction in patients with respiratory muscle weakness.

We investigated pulmonary mechanics in 25 patients, 9 to 55 years of age, with a variety of generalised neuromuscular diseases and variable degrees of respiratory muscle weakness. The average degree of inspiratory muscle force was 39.2% (range 8-83%) of predicted. The lung volume restriction far exceeded that expected for the degree of muscle weakness: the observed decrement in respiratory muscle force should, theoretically, decrease vital capacity to 78% of its control value, while the mean VC in our patients was only 50% of predicted. Analysis of lung pressure-volume curves indicated that the two principal causes of the disproportionate loss of lung volume were a reduction in lung distensibility probably caused by widespread microatelectasis, and a decrease in the outward pull of the chest wall. Because it reflects both direct (loss of distending pressure) and secondary (alterations in the elastic properties of the lungs and chest wall) effects of respiratory muscle weakness on lung function, we conclude that, in these patients, the vital capacity remains the most useful measurement to follow evolution of the disease process or response to treatment.

Adolescent↗

PubMed2000

Factors related to hip muscle weakness following fixation of acetabular fractures.

Two hundred twenty-five acetabular fractures treated surgically by one surgeon using a single surgical approach were reviewed to identify the incidence of clinically significant hip muscle weakness. Clinical grade of fair or poor and presence of radiographic signs of osteoarthritis were most strongly correlated with hip muscle weakness (P<.0001). Other factors related to muscle weakness were >21 days to repair, abdominal trauma, infection, avascular necrosis, heterotopic ossification resection, chest trauma, and head trauma. The presence of arthritis at follow-up increased the incidence of hip muscle weakness (46% [41/89]; P<.0001) independent of surgical approach.

Acetabulum↗

PubMed1977

Pulmonary mechanics in patients with respiratory muscle weakness.

Pulmonary mechanics and respiratory muscle pressures were studied in 7 patients with severe respiratory muscle weakness. Minimal pleural pressures were grossly abnormal and showed little variation with lung volume. Both the maximal transpulmonary pressure and static expiratory compliance were low; therefore, the pressure-volume curves of the lungs resembled those obtained after strapping the chest in normal subjects. The low compliance may result from either microatelectasis or a generalized alteration in alveolar elastic properties and is probably a major determinant of both the total lung capacity and the breathing pattern of patients with neuromuscular disease. Airway and gas exchange function were less abnormal than the elastic properties of the lungs.

Adult↗

PubMed1996

Low serum creatine kinase activity is associated with muscle weakness in patients with rheumatoid arthritis.

OBJECTIVE: In rheumatoid arthritis (RA) serum creatine kinase (CK) is reduced in association with inflammatory response variables. Our objective was to examine whether low CK is associated with muscle weakness and to what extent the hypothesized relationship between CK and muscle weakness can be explained by anthropometric and sociodemographic variables and/or disease variables. METHODS: Cross sectional and longitudinal retrospective analyses of clinical, radiological, and biochemical data of a prospective cohort of consecutive patients with RA. Isometric muscle strength was measured with a validated muscle strength index (MSI); CK was measured with an enzymatic assay (N-acetyl-cysteine, 37 degrees C). RESULTS: 65 patients were enrolled in the study and we obtained complete one year followup data from 47. In cross sectional analysis, CK was a significant, moderate correlate of the MSI (r = 0.43, p < 0.01). CK remained a significant explanatory variable of the MSI in multivariate models that controlled for demographic variables and lean body mass, corticosteroid use, and biochemical, clinical, and radiological disease variables. In longitudinal dichotomous analyses, worsening in CK was weakly but significantly associated with decreased muscle strength, whereas in linear analyses the association did not reach significance. CONCLUSION: In patients with RA, low CK activity is associated with muscle weakness. Demographic, anthropometric, and disease variables related to muscle mass or muscle atrophy explain only part of this association. Our findings support the hypothesis that muscle weakness may be partly caused by a disease related reduction of CK activity independent of muscle atrophy.

Adrenal Cortex Hormones↗

PubMed2000

Effects of creatine supplementation on muscle weakness in patients with rheumatoid arthritis.

BACKGROUND AND OBJECTIVES: Patients with rheumatoid arthritis (RA) frequently suffer from muscle weakness. Oral administration of creatine has been shown to improve muscle strength in healthy subjects. The objective of this study was to examine the effect of oral creatine supplementation on muscle weakness, disease activity and activities of daily living in patients with RA. METHODS: During a period of 3 weeks, 12 patients with RA were treated with creatine monohydrate (20 g/day for 5 days followed by 2 g/day for 16 days). They were examined on entry and at the end of the study. The patients were investigated clinically, blood and urine samples were obtained, muscle biopsies were performed before and after treatment, muscle strength was determined, and self-administered patient questionnaires were completed. RESULTS: From all patients we were able to obtain full clinical and questionnaire data, while biopsies were taken from 12 patients at the start and from nine patients at the end of the study. Muscle strength, as determined by the muscle strength index, increased in eight of 12 patients. In contrast, physical functional ability and disease activity did not change significantly. The creatine concentration in serum and skeletal muscle increased significantly, while creatine phosphate and total creatine did not increase in skeletal muscle. The skeletal muscle creatine content was associated with muscle strength at baseline but not after administration of creatine. The changes in muscle strength were not associated with the changes in skeletal muscle creatine or creatine phosphate. CONCLUSION: Although the skeletal muscle creatine content and muscle strength increased with creatine administration in some patients with RA, a clear clinical benefit could not be demonstrated for this treatment when the patients were considered as one group.

Adult↗

PubMed1999

A novel syndrome of episodic muscle weakness maps to xp22.3.

We describe a family with a novel disorder characterized by episodic muscle weakness and X-linked inheritance. Eight males in three generations demonstrate the characteristic features of the disorder. Episodes of severe muscle weakness are typically precipitated by febrile illness and affect the facial and extraocular musculature, as well as the trunk and limbs, and resolve spontaneously over a period of weeks to months. Younger members of the family are normal between episodes but during relapses show generalized weakness, ptosis, and fluctuations in strength. In some cases, fatigability can be demonstrated. The proband has late-onset chronic weakness and fatigability. The clinical phenotype has features suggestive both of the congenital myasthenic syndromes and of ion-channel disorders such as the periodic paralyses. We have localized the responsible gene to chromosome Xp22.3, with a maximum two-point LOD score of 4. 52 at a recombination fraction of.0, between OACA2 and DXS9985.

Adolescent↗

PubMed1989

Respiratory muscle weakness in the Lambert-Eaton myasthenic syndrome.

Respiratory muscle function was assessed in six patients with the Lambert-Eaton myasthenic syndrome. Five had histologically proved small cell carcinoma of the lung; the sixth later developed metastases from an unknown primary site. Two patients had ventilatory failure, one without respiratory symptoms; another, who had emphysema, had dyspnoea and orthopnoea. The remaining three patients had no respiratory symptoms. Four patients had limb muscle weakness as judged by the maximal voluntary contraction of the quadriceps muscle (range for all subjects 32-100% predicted). Transdiaphragmatic pressure (Pdi) was measured during a maximal unoccluded sniff (Pdi: sniff), a maximal sustained inspiratory effort against a closed airway (Pdi: Pimax), and phrenic nerve stimulation (Pdi: twitch). Mild to moderate diaphragmatic weakness was present in all six patients in proportion to the degree of leg weakness (Pdi: sniff 30-64% predicted; r = 0.6; Pdi:Pimax 6-69% predicted, r = 0.8); this was associated with very low or absent Pdi:twitch during phrenic nerve stimulation. Four patients had weakness of the expiratory muscles. Improvement in muscle strength was documented in two patients after tumour chemotherapy and specific treatment with 3,4-diaminopyridine and prednisolone; one patient was still alive five years from first diagnosis. It is concluded that the respiratory muscles may be implicated in this condition more often than has previously been recognised. As the lack of mobility may cause respiratory symptoms to be minimised, the presence of respiratory muscle weakness may remain undiagnosed unless formal measurement of respiratory muscle function is made.

Autoimmune Diseases↗

PubMedDate not supplied

Electromyographic predictors of residual quadriceps muscle weakness after anterior cruciate ligament reconstruction.

BACKGROUND: Despite the high prevalence of residual quadriceps muscle weakness after anterior cruciate ligament reconstruction, specific predictive factors have not been identified. HYPOTHESIS: Electromyographic analysis is a better predictor of residual muscle weakness than is preoperative strength. STUDY DESIGN: Prospective cohort study. METHODS: The quadriceps muscle strength of 37 patients (25 men, 12 women) was measured before reconstruction and 5 weeks and 6 months after surgery. Quadriceps surface electromyographic signals were recorded during all of the strength tests. Integrated electromyographic analysis and median frequency measurements were computed as deficits on the involved side. Patients also performed a single-legged hop test at the 6-month follow-up examination. RESULTS: The patients had significantly lower strength, integrated electromyographic analysis, and median frequency measurements on the involved side at all three time intervals. The best predictor of the quadriceps muscle strength deficit at 6 months was the combination of the preoperative median frequency deficit and the 5-week postoperative strength deficit. The best predictor of the hop test deficit at 6 months was the combination of preoperative deficits in integrated electromyographic analysis and median frequency. CONCLUSION: Preoperative electromyographic indices of quadriceps muscle function and early postoperative strength were predictive of residual weakness and impaired function 6 months after reconstruction.

Adult↗

PubMed2000

Myoadenylate deaminase deficiency with progressive muscle weakness and atrophy caused by new missense mutations in AMPD1 gene: case report in a Japanese patient.

A 46-year-old woman with exertional myalgia developed slowly progressive weakness in her lower extremities. She had slight muscle weakness in her facial and upper extremities, and severe muscle weakness and atrophy in lower extremities more marked in the proximal portions. Serum creatine kinase was slightly elevated. After ischemic forearm exercise test, blood ammonia had no elevation although lactate level increased normally. The computed tomography revealed that a characteristic distribution of skeletal muscle involvement with proximal and flexor muscles more severely affected than distal and extensor in the lower extremities. In addition, the left sternocleidomastoid muscle showed marked atrophy with an asymptomatic weakness of over 20 years duration suggesting abnormal development. Needle EMG examination showed a large number of easily recruited, short-duration, low-amplitude motor unit potentials in all extremities. Muscle biopsy showed absence of adenosine monophosphate deaminase activity with normal cytochrome c oxidase and phosphorylase activity. With the muscle enzyme activity assay, adenosine monophosphate deaminase activity was found to be lower than 0.2% of the controls. The DNA analysis revealed that she was compound heterozygote involving two missense mutations (R388W and R425H) in exon 9 and exon 10 of AMPD1 gene. This is the first report of primary myoadenylate deaminase deficiency with progressive weakness and atrophy caused by novel compound heterozygous mutations of AMPD1 gene, and suggests that adenosine monophosphate deaminase is closely related not only to energy metabolism but also to the development of skeletal muscle.

AMP Deaminase↗

PubMed1989

[A case of polymyositis with repeated dysphagia and muscle weakness associated with peculiar findings of skin].

A case of polymyositis with repeated dysphagia and muscle weakness associated with peculiar findings of skin was reported. The patient was a 67-year-old man. His birth and development was normal. There was no family history of neuromuscular disease. On 26th March 1987 he was admitted to a hospital because of dysarthria and dysphagia after fever and diagnosed as having viral myositis. His conditions improved spontaneously with bed rest and he left hospital on 14th April. On 23rd April he had chill and sore throat with fever. On 27th he was admitted to the same hospital because of dysarthria and muscle weakness of the proximal portion of the upper limbs. These symptoms also improved with bed rest. He had repeated these symptoms several times and then he was admitted to our hospital on 12th June. On examination he showed the skin pigmentation under the right eye and the eruption in the back of hands and the buttocks. Muscle weakness was observed in the proximal portion of the upper limbs and the neck flexor. Laboratory tests in admission were as follows: sGOT 49 mU/ml, sGPT 104 mU/ml, LDH 1064 mU/ml, CPK 565 mM/ml, aldolase 25.2 IU/1/37 degrees C. Electromyography showed the typical myogenic changes and biopsy of left biceps brachii revealed inflammatory cells in the muscle fiber which are specific to polymyositis. Immuno-histochemical study is performed to analyse the subpopulation of mononuclear cells in biopsied muscle and skin. Mononuclear cells infiltrated into perimysium, endomysium and epidermis were positive for T11 and T8, but less positive for T4, B1 and Leu11. On the basis of these findings he was diagnosed as having "polymyositis syndrome".

Aged↗

PubMed1986

Reversible respiratory muscle weakness in hypothyroidism.

Physiological studies performed 1 week after initiation of thyroid replacement showed persistence of significant respiratory muscle weakness in a patient presenting with hypothyroidism and hypercapnia. Repeat studies 12 months later demonstrated return of respiratory muscle strength to normal. Earlier reports on respiratory failure in hypothyroidism had postulated a critical role for respiratory muscle weakness in the genesis of hypercapnia. Since hypercapnia was rapidly reversed despite the persistence of severe respiratory muscle weakness, this explanation may not be always correct. It appears than in our patient thyroid replacement had its primary effect on the respiratory control system.

Aged↗

PubMed1987

Respiratory muscle weakness and ventilatory failure in AL amyloidosis with muscular pseudohypertrophy.

Generalized muscle weakness culminating in ventilatory failure developed in a 59-year-old man with kappa light chain multiple myeloma. Physical examination demonstrated skeletal muscle enlargement, severe proximal muscle weakness, and macroglossia, consistent with amyloid-associated muscle pseudohypertrophy. Pulmonary function studies revealed a severe restrictive abnormality with a low maximal inspiratory pressure and maximal voluntary ventilation. Arterial blood gas values and chest radiographic results were normal. There was no clinical evidence of cardiac or central nervous system disease. At autopsy, skeletal muscles and diaphragm were diffusely infiltrated by amyloid. There was also multifocal deposition of amyloid in alveolar septae, esophagus, and subendocardium. This report suggests that ventilatory failure may occur as a complication of myeloma-associated (AL) amyloidosis involving the respiratory muscles.

Amyloidosis↗

PubMed2001

Cardiac abnormalities and skeletal muscle weakness in carriers of Duchenne and Becker muscular dystrophies and controls.

Cardiac abnormalities, cardiomyopathy and skeletal muscle weakness have been described in female carriers of the Xp21 (Duchenne and Becker) muscular dystrophies (J Neurol 1975;209(4):279-285; Br Med J 1969;2:418-420; J AmMed Assoc 1996;275(17):1335-1338; Neurology 1980;30(5):497-501; Neuromusc Disord 1999;9:347-351; Arch Neurol 1989;46:673-675). We have screened volunteers from our Xp21 genetics register and found the prevalence of previously unrecognized, clinically relevant, abnormalities in this group to be less than previously reported. We studied 91 women (56 carriers and 35 controls), aged between 18 and 69 years, from our local population known to the Oxford Regional Genetics Register. Our study included controls, with the investigators being blind to the subject's genetic status. The prevalence of previously unrecognised cardiac abnormalities on echocardiogram and ECG was 18% (10/56). Seven percent (4/56) of carriers had cardiomyopathy, defined by significant LV dilatation and decreased shortening fraction. In most cases, subjects with abnormal cardiac findings were asymptomatic. Echocardiography was more frequently abnormal than electrocardiography, but in many subjects the measurements of left ventricular dimensions were only just outside the normal ranges. The prevalence of skeletal muscle weakness was 12% (7/56). It was usually recognized by the individual, although not previously volunteered, but was mild and did not substantially affect activities of daily living.

Adult↗

PubMed1996

The avian low score normal muscle weakness alters decorin expression and collagen crosslinking.

Extracellular matrix development of chicken pectoral muscle was examined in the Low Score Normal (LSN) genetic muscle weakness and compared to both normal and avian muscular dystrophy (MD). At 20 days of embryonic development significant elevations were noted in LSN total glycosaminoglycan concentration and decorin, while at 14 days, LSN glycosaminoglycan and decorin levels were indistinguishable from the controls. Levels of a large skeletal muscle chondroitin sulfate proteoglycan (M-CSPG) appear to be unaffected. Morphologically, at 20 days, the extracellular matrix space between muscle fibers increased to a level characteristic to that observed in avian muscular dystrophy. At six weeks posthatch a marked increase in LSN collagen crosslinking relative to MD or control tissues was observed, while collagen concentration was not altered. By one year posthatch LSN collagen crosslink levels did not significantly differ from normal tissue. These data support the concept that the LSN muscle weakness is associated with changes in both proteoglycan and collagen characteristics.

Animals↗

PubMed2006

Intensive-care-unit-acquired muscle weakness.

Neuromuscular abnormalities culminating in skeletal-muscle weakness occur very commonly in critically ill patients. Intensive-care-unit (ICU) acquired neuromuscular abnormalities are typically divided into 2 discrete classes: polyneuropathy and myopathy. However, it is likely that these 2 entities commonly coexist, with myopathy being the most common cause of weakness. Major risk factors for ICU-acquired neuromuscular abnormalities include sepsis, corticosteroid administration, and hyperglycemia, with other associated factors including neuromuscular blockade and increasing severity of illness. The pathogenesis of these disorders is not well defined, but probably involves inflammatory injury of nerve and/or muscle that is potentiated by functional denervation and corticosteroids. ICU-acquired neuromuscular abnormalities are associated with multiple adverse outcomes, including higher mortality, prolonged duration of mechanical ventilation, and increased length of stay. The only intervention proven to reduce the incidence of ICU-acquired neuromuscular abnormalities is intensive insulin therapy. Additional research is necessary to better delineate the causes and pathogenesis of these disorders and to identify potential preventive and therapeutic strategies. In addition, consensus guidelines for its classification and diagnosis are needed.

Humans↗

PubMed2002

[Generalized muscle weakness mimicking periodic paralysis in a patient with toluene abuse].

A 23-year-old Japanese man was admitted to our hospital because of acute generalized muscle weakness and frequent vomiting. He had been diagnosed as having hypokalemic periodic paralysis, since he had recurrent episodes of transient generalized muscle weakness with a hypokalemia. Laboratory studies have revealed a severe hypokalemic hyperchloremic metabolic acidosis, elevated serum levels of creatine phosphokinase and ammonia. The urinary level of the hippuric acid, a metabolic product of toluene, was found to be extremely high, suggesting that he had been exposed to toluene. With intravenous supplement of potasium, his muscle strength improved. Chronic exposure to toluene induces various neurological disorders, such as encephalopathy, cerebellar and pyramidal signs, peripheral neuropathy. In addition, it should be kept in mind that hypokalemic muscle weakness can be induced by the renal tubular acidosis resulting from chronic toluene exposure, and that it is by no means easy to distinguish hypokalemic periodic paralysis if it occurs recurrently.

Acidosis, Renal Tubular↗