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PubMedDate not supplied

Principle and design of a mobile arm support for people with muscular weakness.

This article describes the development of a mobile arm support for people with muscular diseases. The arm support is spring-balanced, with special attention on reduction of operating effort (high balancing quality and low friction), functionality (large range of motion), and aesthetics (inconspicuous design). The spring settings can be adjusted for wearing heavier clothing or picking up an object, a function that can also be used for moving up or down. The device levels itself automatically to compensate for uneven floors, a function that can be overruled to assist forward/backward motion of the arm. Thus, the balancer can compensate for the weight of the arm and be adjusted to generate force to a limited (safe) extent. The principle and design of the mechanism are presented and preliminary field trial results are given. Two users report on 6 months of continuous use of the arm support in their home and social environments.

Arm↗
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↗
PubMed1982

[Chromosome analysis of swine and their offspring with muscular weakness of the extremities].

The chromosome analysis was used to examine three triads (sire - dam - progeny) and two pairs (sire - dam) after whom the progeny inherited the muscular dystrophy of extremities. In the first case, the examination included the progeny, in the second case only the parents. The examination was performed by using lymphocyte caryotypes of peripheral blood and evaluated by the method after Moorhead et al. (1960) modified by Lojda et al. (1974). Each animal had a separate card. In all animals, hyposomy, hyperploidy and polysomy occurred most frequently, less frequent was the occurrence of breaks. With respect to the variability of the found numerical and structural changes in caryotypes of the examined animals, it was impossible to generalize the specificity of these changes for the muscular dystrophy of extremities in pigs.

Animals↗
PubMed1971

Characteristic clinical findings in some neurogenic myopathies and in some myogenic myopathies causing muscular weakness, hypotonia and atrophy in infancy and early childhood.

Some conditions causing neurogenic or myogenic myopathy are reviewed and illustrated by cases of 1) perinatal cervical cord injury; 2) various types of progressive spinal muscular atrophy and 3) congenital muscular dystrophy, Duchenne-like type of muscular dystrophy, limb-girdle type of muscular dystrophy. All the cases of muscular dystrophy described here occurred in girls.

Adolescent↗
PubMed2000

Deletions in the spinal muscular atrophy gene region in a newborn with neuropathy and extreme generalized muscular weakness.

A newborn presented with respiratory insufficiency requiring artificial ventilation, inability to swallow, lack of spontaneous movements including the facial muscles, and areflexia. Nerve conduction velocities were not recordable. Molecular analysis showed a homozygous deletion in the spinal muscular atrophy (SMN) gene region on chromosome 5q. Pathological and neuropathological examination revealed a normal number of anterior horn cells, hypomyelinated axons in peripheral nerves and some atrophy of skeletal muscle fibres in combination with sarcoplasmic glycogen accumulation. This observation illustrates that severe congenital neuropathy can result from deletions in the SMN gene.

Axons↗
PubMed1994

[Isolated proximal muscular weakness disclosing myasthenic syndrome].

Three cases of chronic limb-girdle myasthenia gravis (one man and two women) are reported. The duration of the disease was three, five and 20 years respectively. None had oculobulbar weakness during this period nor fluctuating symptoms. The primary diagnosis was myopathy in two cases and myelopathy in the other one. In view of this diagnosis, several features were atypical: absence of marked wasting, preservation of tendon reflexes and normal serum creatine kinase activity. Finally, diagnosis of myasthenia gravis was established by the occurrence of a characteristic decremental muscular response to repetitive stimulation and by positive edrophonium test. It seems that the rate of positivity of acetylcholine receptor antibody is lower than in the common form of the disease. Two patients responded to acetylcholinesterase inhibitors and one to high-doses intravenous human immunoglobulins. These and previous cases described in the literature raise the problem of the definition of an unusual form of myasthenia gravis or of a new type of neuromuscular disease characterized by the presence of distinctive changes on muscular biopsies, specially tubular aggregates as in one of our cases. However, this unusual form of chronic limb-girdle weakness has to be recognized because treatments are effective in most cases.

Adult↗