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Results for “Muscle Hypotonia”

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At least 19 recordsLinked to original sources
PubMed2000

Neonatal muscle hypotonia--an early manifestation of cerebral palsy.

UNLABELLED: Cerebral palsy causes a number of diagnostic, therapeutic, organisational, and social problems. A timely diagnosis reduces the unfavourable effects of the disease and the resulting disability of the children. AIM: The aim of the present study was to evaluate the role of the neonatal muscle hypotonia as an early indicative symptom of cerebral palsy (CP). MATERIAL AND METHODS: Forty-two children with clinical and anamnestic data of muscle hypotonia (from the neonatal period to the age of 3) were enrolled in the study. An active and dynamic follow-up including specialized neurologic examinations was realised. RESULTS: The etiologic factors of utmost importance for CP were prematurity (40.5%) and perinatal asphyxia (26.2%). On the background of differently expressed muscle hypotonia, persisting from the neonatal period, the abnormalities in the psychoneurologic development during the first year after birth were characterized mainly by psychoemotional retardation. Motor deficit was marked from the 1st through 2nd year, and speech disorders appeared after the age of 2. CONCLUSIONS: The presence of partial or generalized muscle hypotonia in the neonatal age and its persisting in the subsequent stages of the child's life is an early indicative symptom of CP. The diagnosis is possible within the first two years of life, especially in children with perinatal pathology, by dynamic neurologic follow-up and prompt evaluation of the abnormalities in the psychoneurologic development.

Age Distribution↗
PubMed2006

Hereditary hypotonia, muscle weakness, failure to thrive, and cognitive delay in a large moslem kindred.

Five infants of a Moslem-Arab extended family were evaluated for common and characteristic clinical findings of failure to thrive, extreme muscle weakness, severe motor delay, and moderate to severe cognitive and verbal delay. All children were below the third percentile in weight and height, and three of them had head circumference below the third percentile. Neurologic examination revealed severe hypotonia, muscle weakness, and absent deep tendon reflexes. Two children died at 2 years of age, and none of the children acquired full head control and the motor milestones of rolling and sitting. Laboratory evaluation including muscle biopsies, genetic studies, and metabolic evaluation was nondiagnostic.

Biopsy↗
PubMedDate not supplied

Fiber density in congenital muscle fiber type disproportion. II. Congenital muscle hypotonia and hip dislocation.

Our previous paper presenting electromyographic findings in patients with congenital fiber type disproportion myopathy, confirmed the myogenic character of the disease process. That group of patients was however fairly heterogenous regarding both the clinical features and the morphological changes in muscle fibers (e.g. cases with central cores). In the present study we have examined 13 children with hypotonia and muscle fiber type disproportion operated on in childhood for congenital hip dislocation. In all cases CNEMG and SFEMG with FD estimation was performed in biceps brachii and quadriceps femoris muscles. In all muscles examined either slight EMG changes indicative of myopathy or a normal EMG pattern was found. None of the patients demonstrated an evident increase in FD values. Normal FD and the recruitment pattern proportional to the force of contractures indicate that the normal number of motoneurons is preserved. Accordingly, our present findings confirm the conclusions of our previous paper.

Adolescent↗
PubMed1992

[Control of isometric muscle contraction in muscle hypotonia of central origin: EMG mapping analysis].

Electromyographic and mechanographic investigations in patients with muscular hypotonia, which is, for instance, a side-effect after stereotactic treatment of tremor syndromes, permit the presumption that in this sensomotor open-loop situation the decreased muscular resistance to stretching during isometric contraction (initial stiffness) is caused by changes of muscular innervation pattern. Probably, the innervation pattern during tonic activity is changed by a shift of a more tonic motoneurone behaviour to motoneurone activities with predominantly phasic characteristics. In 17 controls and 4 patients with muscular hypotonia caused by stereotactic lesions of VIM area (treatment of tremor syndromes) the EMG of right and left side forearm flexors (especially the activity of the M. biceps brachii) was investigated by a sophisticated, topographically oriented 16-channel-surface-EMG-technique ("EMG-Mapping") during slight isometric contraction. EMG-Maps of forearm flexors (especially of M. biceps brachii) in patients with centrally evoked muscular hypotonia demonstrate that in these open-loop conditions the motor control is changed. For this the reason could be a shift of the activated motor units from a predominantly static to a more phasic functional behaviour. The latest results on muscular activation processes in cats support this presumption.

Adult↗
PubMed1991

[Respiratory muscle hypotonia as one of the causes of hypoventilation and hypoxemia in patients with chronic renal failure treated by hemodialysis].

In 21 patients with chronic renal failure spirometric and electromyographic (included m. pectoralis, m. rectus abdomini, m. obligus abdomini) examinations were performed before and after hemodialysis. We observed a decreased myoelectrical activity of muscles on the basis of amplitude of EMG. Weakness of the respiratory muscles may be one of the causes of hypoventilation and hypoxemia during hemodialysis.

Abdominal Muscles↗
PubMed1991

[Analysis of the causes of respiratory muscle hypotonia in patients with chronic renal failure treated by peritoneal dialysis and hemodialysis].

In 21 patients with chronic renal failure spirometric and electromyographic examinations (including m. pectoralis, m. rectus abdomini, and m. obligus abdomini) were performed before and after hemodialysis. In 10 patients treated by peritoneal dialysis and, in 35 patients treated by hemodialysis serum PTH, thyroid hormones (T4, T3, rT3), CPK, aldolaze, pyruric acid, lactic acid, alkaline phosphatase were determined. In both groups before and after dialysis serum sodium, potassium, calcium, magnesium were determined. We observed negative correlation between PTH and respiratory muscles weakness indices. This fact may confirm the contribution of PTH in uremic myopathy evaluation.

Abdominal Muscles↗
PubMed1983

Multiple acyl-Co A dehydrogenation deficiency (MADD) in a boy with nonketotic hypoglycemia, hepatomegaly, muscle hypotonia and cardiomyopathy. Detection of N-isovalerylglutamic acid and its monoamide.

A boy, aged 7 months, of consanguineous parents presented with an acute onset of vomiting, fever, nonketotic hypoglycemia and acidosis and died from cardiac arrest after ventricular fibrillation. He had hepatomegaly and echocardiographically a non-obstructive cardiomyopathy. Autopsy was not allowed. After birth the child had suffered from a severe respiratory distress syndrome, transient metabolic acidosis and had a sweaty feet odour. Later on, development was retarded with a severe muscular hypotonia. Post mortem, numerous unusual organic acids were found in high concentrations in urine, e.g. dicarbonic acids, 2-hydroxyisobutyric, isovaleric, 3-hydroxyisovaleric acid, N-acyl glycines, isovalerylglutamic acid and sarcosine. This pattern indicated deficiencies of several acyl-Co A dehydrogenases in the metabolism of leucine, isoleucine, valine, lysine, short-chain fatty acids and sarcosine. This could be confirmed using cultured skin fibroblasts which were shown to degrade the corresponding labeled substrates insufficiently to 14CO2. It is assumed that the functional multiple acyl-Co A dehydrogenation deficiency is caused by a deficiency of a common link in the electron transfer system of these dehydrogenases which is inherited autosomal recessively in this family. Among the 12 patients reported, 7 died within the first 5 days of age.

Cardiomyopathies↗
PubMed1991

Type III collagen deficient EDS IV producing muscular hypotonia with abnormal muscle fibroblasts.

Muscle biopsy and fibroblast culture of a floppy child with Ehlers-Danlos syndrome type IV were studied. Biochemical analysis of the tissue showed drastically reduced amount of collagen type III. Electron microscopic examination of muscle as well as of cultured fibroblasts showed grossly dilated and dominated the cytoplasm endoplasmic reticulum. Dilatation may result from storage of an abnormal collagen type III molecule. Our observations indicate that type III collagen deficiency may be present clinically as a congenital muscle hypotonia. Specific ultrastructural abnormalities of fibroblasts found in muscle biopsy can enable the proper diagnosis.

Child↗
PubMed1977

Acute fulminant myoglobinuric polymyositis with picornavirus-like crystals.

Myoglobinuria was found in an 11 month old girl suffering from fever, dyspnoea, and muscle hypotonia. Muscle biopsy showed focal degenerative necrosis of the muscle fibres. Electronmicroscopically, picornavirus-like crystals were demonstrated in the muscle fibres. These and other findings strongly suggest that she suffered from acute myositis with myoglobinuria probably caused by Coxsackie B6 virus infection. The causal relationship of viral infection (Coxsackie, influenza, or myxo-viruses) and acute or chronic polymyositis with or without myoglobinuria is discussed.

Acute Disease↗
PubMed1978

Delay in the maturation of muscle fibers in infants with congenital hypotonia.

Muscle biopsies of hypotonic children have shown delayed maturation of a fetal type of muscle fibers: subsarcolemmal halo devoid of activity for mitochondrial dehydrogenases, type II predominance and in some cases abnormal dispersion of fiber diameter. Fiber subtypes within group II were also abnormal. One case has definite embryonic characteristics with presence of myoblasts. Not a single clinical pattern was present in these patients and a variety of associated disorders were recognized. Some patients had a clinical picture corresponding to congenital benign hypotonia as described by Walton.

Child, Preschool↗
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↗