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At least 199 records · Page 11Linked to original sources
PubMed2000

Diabetes mellitus, deafness, muscle weakness and hypocalcemia in a patient with an A3243G mutation of the mitochondrial DNA.

In a 54-year-old woman with diabetes mellitus, hearing loss, muscle weakness and hypocalcemia, caused by idiopathic hypoparathyroidism, an A to G transition at the nucleotide position of 3243 (A3243G mutation) was found in the mitochondrial DNA from her leukocytes. Clinical features of diabetes mellitus and hearing loss in association with the A3243G mutation are compatible with a diagnosis of maternally inherited diabetes and deafness (MIDD). Although hypoparathyroidism is rarely seen in MIDD, we consider that hypoparathyroidism in this patient is a possible phenotype caused by the A3243G mutation of mitochondrial DNA.

Calcium↗
PubMed1992

Rigid spine syndrome with selective respiratory muscle weakness.

Rigid spine syndrome is a rare myopathy characterized by mild axial and proximal muscle weakness, limitation of neck and trunk flexion, scoliosis and mild joint contractures. We describe a 20-year-old woman with this syndrome who developed severe respiratory muscle failure disproportionate to the well-preserved extremity muscles. Nocturnal home care ventilation has completely restored her arterial oxygen desaturation during a 5-year follow-up.

Adult↗
PubMed1997

Disturbances of neuromuscular interaction may contribute to muscle weakness in spinal muscular atrophy.

During a critical period of development, motoneurones and muscles are dependent on functional interaction with each other for their survival. In certain neuromuscular disorders such as spinal muscular atrophy (SMA), motoneurones die and muscle development is seriously affected. Recently advances have been made towards understanding the genetic basis of this disease, and a particular gene, i.e. the survival motoneurone gene (SMN), has been identified and found missing in SMA patients. Nevertheless the function of this gene is not clear, it may be involved in the control of the development of either the motoneurone or the muscle. Here we report that disrupting neuromuscular interaction during the early postnatal period has similar consequences on the development of muscles and motoneurones to those seen in patients with SMA, in that there is a loss of motoneurones and muscle function is severely impaired. In view of this, we discuss the possibility that these symptoms in SMA patients may be due to a disturbance of neuromuscular interaction during a critical stage of development.

Animals↗
PubMed2001

Muscle weakness in Parkinson's disease: a follow-up study.

We compared isokinetic muscle strength between initial and subsequent measurements in 10 patients who could repeat the same testing later among 23 previously described patients with Parkinson's disease. Patients were divided into two groups according to changes in clinical condition between the times of the first and the subsequent measurements. For patients who had improved, both extension and flexion on the more affected side showed significantly greater torque at 15 rpm in the later than the earlier measurement. For patients who had worsened, both extension and flexion on the more affected side showed significantly less torque at 5 and 15 rpm in the later than the earlier measurement. Although isokinetic muscle strength is likely to depend on movement velocity in the early stages of Parkinson's disease, it may be influenced by bradykinesia, as the disease progresses. Speed-force correlation seen in these patients may give clues to the understanding of the pathophysiology of bradykinesia.

Aged↗
PubMed2001

Isolated late-onset cone-rod dystrophy revealing a familial neurogenic muscle weakness, ataxia, and retinitis pigmentosa syndrome with the T8993G mitochondrial mutation.

PURPOSE: To report a late-onset cone-rod dystrophy that revealed a familial neurogenic muscle weakness, ataxia, and retinitis pigmentosa syndrome as a consequence of the T8993G mitochondrial mutation. METHODS: Observational case series. A 42-year-old female disclosed a late-onset retinal dystrophy. The family history revealed that her three sons, one of them deceased at the age of 4, had mental and neurologic impairment of variable severity. The retinal dystrophy of the mother was classified as a cone-rod dystrophy. Retinal dystrophy was subsequently diagnosed in the two surviving sons. Screening for mutation in the mitochondrial DNA (mtDNA) was performed because of the combination of neurologic involvement and retinal dystrophy in this family. RESULTS: Molecular analysis of the mtDNA revealed the ATPase-6 gene T8993G mutation in the mother and the two sons. CONCLUSION: This family illustrates the remarkably variable expression of retinal and systemic manifestations related to the T8993G mutation ranging from an isolated late-onset cone-rod dystrophy to a severe neurodegenerative process with a dramatic outcome. Genetic counseling for retinal dystrophies requires careful evaluation of the familial medical history.

Adenosine Triphosphatases↗
PubMed2006

Muscle weakness: a progressive late complication in diabetic distal symmetric polyneuropathy.

The aim of the study was to determine the progression of muscle weakness in long-term diabetes and its relation to the neuropathic condition. Thirty patients were recruited from a cohort of 92 diabetic patients who participated in a study on muscular function 6-8 years earlier. Nine subjects were nonneuropathic, 9 had asymptomatic neuropathy, and 12 had symptomatic neuropathy. Thirty matched control subjects who participated in the initial studies were also included. At follow-up, isokinetic dynamometry at the ankle, electrophysiological studies, vibratory perception thresholds, and clinical examination (neuropathy symptom score and neurological disability score [NDS]) were repeated. The annual decline of strength at the ankle was 0.7 +/- 1.7% in control subjects, 0.9 +/- 1.9% in nonneuropathic patients, 0.7 +/- 3.1% in asymptomatic neuropathic patients, and 3.2 +/- 2.3% in symptomatic neuropathic patients. In the symptomatic patients, the decline of muscle strength at the ankle was significant when compared with matched control subjects (P = 0.002) and with the other diabetic groups (P = 0.023). Also, the annual decline of muscle strength at the ankle was related to the combined score of all measures of neuropathy (r = -0.42, P = 0.03) and to the NDS (r = -0.52, P = 0.01). In patients with symptomatic diabetic neuropathy, weakness of ankle plantar and dorsal flexors is progressive and related to the severity of neuropathy.

Adult↗
PubMed1998

A case of respiratory muscle weakness due to cytochrome c oxidase enzyme deficiency.

Mitochondrial myopathy is a rare cause of dyspnoea and respiratory failure, usually presenting in infancy. We describe a 27 yr old woman with a partial cytochrome c oxidase enzyme deficiency causing respiratory muscle weakness and respiratory failure. The onset was acute, with no preceding respiratory symptoms. The patient was successfully treated with bilevel positive airway pressure therapy.

Adult↗
PubMed1998

Voluntary muscle weakness and co-activation after chronic cervical spinal cord injury.

Muscle strength was assessed from the maximum force that could be exerted voluntarily by triceps brachii muscles of 72 people with chronic cervical spinal cord injury (SCI) at or above C7, and 18 able-bodied (A-B) subjects. The magnitude of co-activation was estimated from the ratio of biceps brachii surface EMG to triceps plus biceps brachii surface EMG (biceps EMG/ triceps + biceps EMG). Maximum voluntary forces exerted by triceps brachii muscles of SCI subjects were significantly lower than those of controls (p < 0.01). Strength differences between muscles of SCI men and women were not evident. Significant positive relationships were found (linear or curvilinear) between triceps surface EMG and force for all control muscles (n = 19) and for 54% of the muscles of SCI subjects (n = 73). The remaining muscle of SCI subjects (n = 63) were either so weak that only one EMG and force value could be measured or EMG occurred without detectable force. For control muscles (n = 19), the mean triceps-biceps EMG ratio was 0.15+/-0.05 for all voluntary contraction force levels. For muscles of SCI subjects, 41 had EMG ratios similar to those of controls, co-activity largely attributed to EMG cross talk; 19 muscles had constant EMG ratios, but these were three standard deviations above the control means; 13 muscles had EMG ratios that decreased or increased as force increased. Muscles of SCI subjects with greater than control levels of co-activity during maximum voluntary contractions (high EMG ratios) were as strong as muscles with EMG ratios similar to controls. These results provide quantitative descriptions of voluntary muscle weakness after SCI and a database from which to evaluate improvements in muscle strength. These data also show that, for many SCI subjects, any triceps-biceps co-activation is similar to that of controls and does not necessarily distort muscle control unduly.

Adult↗
PubMed1998

Muscle weakness in Parkinson's disease: isokinetic study of the lower limbs.

Isokinetic strength of knee extension and flexion was measured at two speeds of movement in 23 patients with Parkinson's disease, to clarify whether muscle weakness is inherent to the disease. To counteract normal variation among subjects, we selected patients with symptoms completely or largely confined to one side and compared sides for each patient. The affected side was weaker than the other in both slow and fast movements early in the disease. In more advanced disease, the difference between sides diminished at the slow speed but remained significant at the faster speed. These observations suggest that weakness is inherent to Parkinson's disease and influenced by movement speed.

Aged↗
PubMed2001

Facial and skeletal malformations, mental retardation, aganglionosis, and neurogenic muscle weakness: a variant of Niikawa-Kuroki syndrome or a new syndrome?

We report a 10-year-old boy with multiple congenital anomalies/mental retardation syndrome, who also presented with aganglionosis and neurogenic muscle weakness. Some phenotypic manifestations of our patient overlap with those observed in the Niikawa-Kuroki syndrome; however, the hypothesis of a new distinct entity, with simultaneous involvement of the central and peripheral nervous system, is considered.

Abnormalities, Multiple↗
PubMed2005

Acute motor and sensory axonal neuropathy (AMSAN) in a 15-year-old boy presenting with severe pain and distal muscle weakness.

Acute motor and sensory axonal neuropathy (AMSAN) is a recently described subtype of Guillain-Barré syndrome characterized by acute onset of distal weakness, loss of deep tendon reflexes and sensory symptoms. Electrophysiological studies show mildly reduced nerve conduction velocities combined with a marked reduction of muscle action and sensory nerve action potentials. Here, we report a 15-year-old boy who suffered from severe burning and knife-like pain that increased over a period of three months and resulted in a disrupted sleep pattern and suicidal intentions as well as marked loss of weight. In addition, he developed muscle weakness in his hands and feet. Neurophysiological and histopathological studies revealed AMSAN. Marked improvement of his condition was achieved by treatment with intravenous immunoglobulins, high-dose methylprednisolone, and a combination of gabapentin, antidepressants, and an oral morphine.

Adolescent↗
PubMed2006

Ectopic adrenocorticotropic hormone syndrome in a case of small cell carcinoma of the bladder manifesting as severe muscle weakness.

Ectopic adrenocorticotropic hormone syndrome is a paraneoplastic syndrome associated with small cell carcinoma. However, ectopic adrenocorticotropic hormone syndrome is rare in association with small cell carcinoma of the bladder. We report what we believe to be the first case of ectopic adrenocorticotropic hormone syndrome associated with small cell carcinoma of the bladder that manifested as severe muscle weakness due to hypokalemia. An early diagnosis and aggressive potassium replacement is essential for retaining muscle strength. The patient died of pneumonia less than 2 months after the diagnosis. Severe immunosuppression by excess cortisol production was suspected. Control of cortisol levels before chemotherapy might be beneficial in preventing infective complications.

ACTH Syndrome, Ectopic↗
PubMed1994

Proximal myotonic myopathy: a new dominant disorder with myotonia, muscle weakness, and cataracts.

We describe three families with a dominantly inherited disorder. Affected individuals have myotonia, proximal muscle weakness, and cataracts. There was no abnormal CTG repeat expansion of the myotonic dystrophy (DM) gene in DNA from blood and muscle. The structure of the three families permitted linkage analysis, and there is no linkage to the gene loci for DM or to the loci for the muscle chloride channel disorders or muscle sodium channel disorders. The collection of symptoms in these three families seems to represent a new disorder.

Adult↗
PubMed2004

Quadriceps femoris muscle weakness and activation failure in patients with symptomatic knee osteoarthritis.

PURPOSE: Quadriceps weakness is common in patients with knee osteoarthritis (OA), and has been attributed to failure of voluntary activation. Methodological differences may have contributed to previous reports of extensive failure of voluntary activation in patients with osteoarthritis. The purpose of this study was to determine the extent of quadriceps muscle weakness and activation failure in middle aged patients with symptomatic medial knee osteoarthritis using maximum voluntary isometric contractions (MVIC) and a burst superimposition technique. METHODS: Measurements of quadriceps MVIC and extent of voluntary activation were made in 12 subjects with knee OA and 12 similarly aged uninjured subjects. Voluntary activation was tested by superimposing a train of electrical stimulation on a maximal effort volitional contraction of the quadriceps muscle. RESULTS: The group of subjects with knee OA had significantly less quadriceps strength relative to body mass index (BMI) than the group of control subjects (p=0.010). No difference in voluntary activation was observed (p=0.233), however, 50% of the OA group, and only 25% of the control group failed to fully activate the quadriceps. DISCUSSION: The finding of quadriceps weakness is consistent with past literature. Providing adequate instruction, feedback, and several attempts to maximally contract the muscle likely yielded greater volitional activation (thus less activation failure) than had been reported previously. This finding has implications for the rehabilitation of weakened quadriceps in patients with knee osteoarthritis.

Adult↗
PubMed1996

Peripheral muscle weakness contributes to exercise limitation in COPD.

Recently, it was suggested that fatigue of peripheral muscles could contribute to exercise limitation in patients with chronic obstructive pulmonary disease (COPD). In order to quantify the role of peripheral muscle force, we restudied potential determinants of exercise capacity (6-min walking distance [6 MWD] and maximal oxygen consumption [V02max]) in 41 consecutive COPD patients (FEV1, 43 +/- 19% of predicted, TLCO, 56 +/- 25% of predicted) admitted to our pulmonary rehabilitation program. VO2max (incremental cycle ergometer test), 6 MWD (best of three), lung function (FEV1, FVC, TLC, FRC), diffusing capacity (TLCO), isometric quadriceps force (QF), hand grip force (HF), and maximal inspiratory (PImax) and expiratory (PEmax) pressures were measured. Patients had a poor 6 MWD (372 +/- 136 m) and VO2max (1.35 +/- 0.60 L, 71%), reduced respiratory (PImax 65 +/- 27%) and peripheral muscle force (QF 74 +/- 27%, HF 82 +/- 23%). In single regression analysis, significant correlations (r) were found for VO2max and TLCO (0.68), FEV1 (0.64), QF (0.55), HF (0.53), and body weight (0.49). Walking distance was significantly correlated with QF (0.63), HF (0.61), PImax (0.49), and TLCO (0.38). In stepwise multiple regression analysis, the variables significantly contributing to 6 MWD were QF and Plmax. For VO2max, variables significantly contributing were TLCO, QF, and FEV1. We conclude that lung function and peripheral muscle force are important determinants of exercise capacity in COPD.

Body Weight↗
PubMed1995

Electromyographic effects of fatigue and task repetition on the validity of estimates of strong and weak muscles in applied kinesiological muscle-testing procedures.

The study investigated the effects of fatigue and task repetition on the relationship between integrated electromyogram and force output during subjective clinical testing of upper extremity muscles. Muscles were studied under two conditions differing in the nature and duration of constant force production (SHORT-F) and (LONG-F). The findings included a significant relationship between force output and integrated EMG, a significant increase in efficiency of muscle activity with task repetition, and significant difference between Force/integrated EMG ratios for muscles labeled "Strong" and "Weak" in the LONG-F condition. This supports Smith's 1974 notion that practice results in increased muscular efficiency. With fatigue, integrated EMG activity increased strongly and functional (force) output of the muscle remained stable or decreased. Fatigue results in a less efficient muscle process. Muscles subjectively testing "Weak" or "Strong" yield effects significantly different from fatigue.

Adult↗