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Results for “Muscular weakness”

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At least 19 recordsLinked to original sources
PubMed1976

A syndrome of widened medullary cavities of bone, aortic calcification, abnormal dentition, and muscular weakness (the Singleton-Merten syndrome).

Two patients with clinical and radiological features similar to those of Singleton and Merten's patients are described. These patients exhibit features of a unique clinical syndrome of unknown etiology: generalized muscular weakness with secondary hip and foot deformities, progressive calcification of the thoracic aorta beginning in childhood, calcific aortic stenosis leading to heart failure, dysplasia of the teeth, poor physical development, osteoporosis, expanded medullary cavities of the metacarpal and metatarsal bones, and chronic psoriaform skin lesions.

Adolescent↗
PubMed1977

[Exercise-induced muscular weakness, myalgia and contractures. I. A clinical review].

In the differential diagnosis of intermittent claudication some rare myopathies have to be considered. The most frequent is phosphorylase deficiency (McArdle's disease). Exercise-induced muscular pain, weakness, contractures and occasionally myoglobinuria are the most prominent clinical signs. Serum creatine phosphokinase, aldolase and lactic dehydrogenase may be elevated after exertion. In the ischemic forearm test there is no rise of serum lactic acid. The enzyme deficiency can be demonstrated by histochemical and biochemical examination of a muscle specimen. Further, but more infrequent, enzymatic disturbances of glycolysis are phosphofructokinase deficiency and phosphohexoisomerase inhibitor, which also yield an abnormal ischemic forearm test and must be demonstrated histochemically and biochemically. Apart from muscular signs, myopathy with lactic acidosis is associated with palpitation, dyspnea and exhaustion, and a disproportionate rise in serum lactic acid level after exertion. Histochemically and electronmicroscopically demonstrable fat accumulation in the muscle can be a sign of a disturbance in lipid metabolism. This type of exercise-induced myopathy has been reported only in a few cases with carnitine-pylmityltransferase deficiency, which has to be demonstrated biochemically. Muscular contractures also exercise-induced but painless and reversible within seconds may be due to deficient uptake of sarcoplasmic calcium in the tubular system. Dyskalemic paralysis causes painless paresis within minutes of hours after exertion, which disappears within hours to a few days. Myopathy with tubular aggregates can be differentiated from other exercise-induced myopathies by morphology. Myotonia combined with painful contractures characterizes myopathia myotonica.

Acidosis↗
PubMed1978

Transient muscular weakness in severe recessive myotonia congenita. Improvement of isometric muscle force by drugs relieving myotomic stiffness.

The maximum force of voluntary muscle contraction was registered under isometric conditions in nine patients with recessive myotonia congenita. The recordings were made on the upper arm. Five patients with severe myotonia had a transient weakness after muscle rest. Electromyographic registrations with wire electrodes showed that the myotonic muscle fiber discharges disappeared during the transient weakness. Medication improving myotonic stiffness also improved the weakness. The cause of transient weakness seems to be similar to that of myotonic stiffness. It is known that an increasing depolarization of the myotonic muscle fiber membrane leads to the myotonic discharges and myotonic stiffness. In severe myotonia the progressing depolarization could cause a loss of excitability of the muscle fiber membrane and thereby a transient paresis of a more or less large number of muscle fibers.

Adult↗
PubMed1978

Dystrophia myotonica and hypothyroidism.

Two cases of dystrophia myotonia associated with hypothyroidism are reported. This association is not frequent. In both cases the hypothyroidism precipitated an otherwise mild muscular weakness due to dystrophia myotonia. Treatment with dried thyroid improved the muscular power, while the myotonia remained unchanged. Since dystrophia myotonica and hypothyroidism have many presenting symptoms in common, a complete assessment of the thyroid function in every case of dystrophia myotonica seems worthwhile.

Electromyography↗
PubMedDate not supplied

Weakness from magnesium-containing cathartics: electrophysiologic studies.

The case history of a patient with severe muscular weakness resulting from magnesium intoxication following oral and rectal administration of magnesium citrate cathartics is reported. The findings of the electrophysiologic studies were characteristic of the neuromuscular blockade seen in this disorder, including marked reduction in evoked muscle action potential amplitude which progressively decline on nerve stimulation at low rates, and a striking degree of facilitation of evoked muscle action potential after exercise or on high-frequency stimulation. When the hypermagnesemia was corrected, strength returned to normal.

Action Potentials↗
PubMed1975

Degeneration of muscle in association with carcinoma of the bronchus.

The clinical features and necropsy findings are described in three cases in which severe and rapidly progressive muscle weakness developed in association with carcinoma of the bronchus. In all three cases, muscular weakness was directly responsible for death. Histological and ultramicroscopical examination in all cases showed an unusual type of degeneration of muscle fibres accompanied by degeneration of intramuscular nerve fibres, but without involvement of the central nervous system, or of the peripheral nerve trunks. The findings are compared with those of previously reported cases, and possible mechanisms for the muscle degeneration are discussed.

Aged↗
PubMed1979

Potentiation of neuromuscular weakness in infant botulism by aminoglycosides.

A retrospective study of ten patients with infant botulism who received gentamicin or kanamycin suggests that aminoglycoside antibiotics potentiate muscular weakness and precipitate respiratory failure as late as 27 days after onset of the disease. Although it is difficult to separate progression of the disease from the effects of antibiotics, the rapidity of deterioration following aminoglycoside treatment and the rapidity of recovery following cessation of aminoglycoside therapy is highly suggestive. A review of five patients who received only penicillin or a semisynthetic derivative of penicillin did not reveal any temporal deterioration with onset of penicillin therapy or improvement with cessation of penicillin therapy.

Ampicillin↗
PubMed1977

Adult-onset acid maltase deficiency. Case report of an adult with severe respiratory difficulty.

Pompe's disease (acid maltase deficiency) classically affects infants and children, with a few sporadic cases occurring in adults. An adult patient initially have progressive muscular weakness, exertional dyspnea, diaphragmatic paralysis, and objective evidence of restrictive respiratory disease. Muscle biopsy established the diagnosis of acid maltase deficiency. The patient's brother had died at the age of 44 years, after 23 years of a "progressive muscular dystrophy." Acid maltase deficiency should be considered in the differential diagnosis of progressive respiratory insufficiency associated with weakness.

Adult↗
PubMed1979

[Hypothyroid myopathy: histochemical and ultrastructural features with physiopatological correlations (author's transl)].

The Authors describe an adult case of hypothyroid myopathy which occurred after a Hashimoto's thyroiditis. Ultrastructural examination of the deltoid muscle showed two fundamental changes: 1) large collections of mitochondria generally normal in shape, structure and size, especially in the subsarcolemmal sapce of the muscle fibre; 2) glycogen deposits both beneath sarcolemmal membrane and between myofibrils. Histochemical examination reveals an increased activity of mitochondrial oxydative enzymes, such as NADPH and SDH especially in subsarcolemmal regions of many type I fibres. The histogram is normal. It seems that the multiplication of skeletal muscle mitochondria may be compensatory to the slowing down of metabolic activities. This, however, is ineffective because it involves the mitochondria localized more superficially in the fibres with a loosely coupled oxydative phosphorylation. Glycogen accumulations are probably due to deficiency of the thyroid hormone; in fact stimulation of carbohydrate metabolism by thyroxine is well known. The abnormal functioning of the muscular mitochondria and the defective utilisation of glycogen are the most important factors in the pathogenesis of muscular weakness of hypothyroid myopathy.

Adenosine Triphosphatases↗
PubMed1978

Weakness, neuropathy, and coma following total parenteral nutrition in underfed or starved rats: relationship to blood hyperosmolarity and brain water loss.

The continuous infusion of a concentrated, high-caloric glucose solution intravenously into underfed or 3-day-starved rats at a rate of 390 kcal/kg/day results in hypophosphatemia, muscular weakness, neuropathy, lethargy, occasional convulsions, and eventual coma and death. This sequence of events is not observed in similarly infused normal rats. It is a model of a fatal parenteral nutrition syndrome which occurs in undernourished patients. Rats in coma had an eightfold increase in the blood glucose level, a 1.6-fold increase in serum osmolarity, a 16% to 20( decrease in brain water content, and normal blood ketones. A lag phase of at least 8 hr and often 12 to 24 hr occurred following the start of the hyperosmotic glucose infusion before the blood glucose began to accumulate progressively and the syndrome developed. The onset of the syndrome could be prevented by the administration of large amounts of insulin required to keep the blood sugar from exceeding 250 mg/dl. Thus the rat model of the fatal hyperalimentation syndrome is a form of hyperglycemic, hyperosmolar, nonketotic coma caused by brain dehydration.

Animals↗
PubMed1979

[Lipidic myopathy with severe cardiomyopathy caused by a generalized carnitine deficiency. Favourable course during carnitine hydrochloride treatment].

The case of a girl who presented with gastrointestinal upsets with nausea, vomiting and occasional hypoglycaemic attacks during childhood is reported. At about 5 years of age generalised muscular weakness with severe amyotrophy, cardiomegaly with a cardiothoracic ratio of 0,63, left ventricular hypertrophy on electrocardiography and left ventricular dilatation with hypokinesis on echocardiography were observed. A few weeks later she developed severe cardiac failure. Muscle biopsy showed muscular dystrophy with lipid infiltration due to carnitine deficiency )serum carnitine 9 nmoles/ml, normal values: 46 +/- 6,9 nmoles/ml; muscle carnitine 0,27 nmoles/mg, normal values: 3,0 +/- 0,79 nmoles/mg fresh frozen weight). She improved rapidly with carnitine chlorhydrate and a diet low in lipids and high in medium chain triglycerides. Regression of muscular symptoms and cardiac failure was observed. After 13 months follow-up with no tonicardiac therapy she is much improved; the signs of heart failure have disappeared, the cardiothoracic ratio is now 0,55 and the electrocardiogramme and echocardiogramme are normal.

Biopsy↗
PubMed1979

The otolaryngologic presentation of myasthenia gravis.

Myasthenia gravis is a neuromuscular disease of insidious onset, characterized by weakness and fatigability of voluntary muscles. Most patients present with symptoms relating to the head and neck and thus may be seen first by the otolaryngologist. Predominant symptoms may be ocular (ptosis or diplopia) or related to fatigue of the oropharyngeal or laryngeal musculature (dysarthria, dysphonia, or dysphagia). Alleviation of muscular weakness and fatigability after administration of anticholinesterase drugs is pathognomonic of myasthenia gravis.

Adolescent↗
PubMed1978

[The vessels of the inner ear (author's transl)].

The inner ear as an example of a highly specialized sensory organ also possesses a highly specialized vascularisation. This represents an impressive example for a reasonable adaption of the terminal blood vessels to a specific function of the organ fulfilling more than only the nutrition. In this paper the microvascular bed of the cochlea is examined using both the injection method of the vessels and the biomicroscopic observation in vivo. The combination of these technics supported by histologic and stereoscan microscopic examinations has made it possible to give an account of the functional morphology of the inner ear vessels. As a detailed structural analysis of the vessels morphology with the help of dyes that fill the whole of the vessels space (i.e. Berlin blue) is not possible, perfusion experiments with silver nitrate were performed on the inner ear. After the perfusion the vessels are cleaned again, the silver however imbibes the intercellular reticular substances and after exposure produces a continous and sharp framework of the endothelium and--when present--muscular cells, thus showing the angioarchitectural contours. There is a very clear division of the cochlear vessels in a three dimensional space: The arterial and venous vessels are vividly separated from one another, forming two systems of microvascular units in the lateral wall and the spiral lamina. Each unit begins with special blood vessel convoluts in the modiolus, consisting of loops of arterioles. They are weakly muscularized whereas no muscle structures are seen elsewhere in the other parts of the inner ear vessels. There are no a.-v. anastomoses or sphinkters at all. The function of the vessel loops in the modiolus is to flatten the pulse wave as well as to regulate the blood flow in the microvascular bed by vasomotion. This was proved by statistical examinations of 1200 measurements of the widths of the vessels at several points of the cochlea in a blind study with and without vasoactive drugs. The terminology of the vessels is not standardized. The nomenclature in this paper has regard to the classification of the vessels, the course and the topographic localisation. Silver staining reveals changes in the form of the endothelium cells from the arterial towards the venous end. While the arteries show a long stretched spinle or lancet like form they change over blunt, oval, triangular or rhomboid forms into polygonal cells with spiked border lines at the venules. All experiments together give an account that the blood supply of the inner ear is in close correlation with the blood supply of the brain and too possesses autoregulative mechanisms, which must be localized in the convoluts at the beginning of every microvascular unit of the cochlear vessels.

Arterioles↗