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At least 325 records · Page 18Linked to original sources
PubMed1977

Catecholamine-induced muscle weakness.

Infusions of epinephrine or levarterenol bitartrate into a rabbit nerve-muscle preparation decreased the force of the evoked twitch of anterior tibial and gastrocnemius-soleus muscles. The adverse effect of the catecholamines was not directly on skeletal muscle. The alpha-receptor blocking drug phenoxybenzamine hydrochloride prevented the adverse effect of the catecholamines if it was given prior to catecholamine infusions and unmasked a weak augmentation of twitch tension. Taken with the finding of abnormal accumulation of catecholamine in human dystrophic muscles, the production of an experimental myopathy resembling human dystrophy by the monoamine oxidase inhibitor pargyline hydrochloride, and the finding of excessive levels of catecholamines in the tissues and urine of dystrophic animals, these experiments support the hypothesis that catecholamines could play a pathogenetic role in some dystrophic diseases of muscle.

Action Potentials↗
PubMed1995

Muscle weakness during tricaine anesthesia.

An isolated preparation of tadpole tail muscle was used to assess the peripheral effects of tricaine (3-aminobenzoic acid ethyl ester) at anesthetic concentrations and under physiological conditions. The drug effect on the electrically-evoked twitch was tested using short-pulse durations that elicited synaptically mediated effects or longer-duration pulses that stimulated the muscle directly. Tricaine reduced both types of response anesthetic and even subanesthetic concentrations. At steady state concentrations that produced surgical anesthesia in vivo, tricaine reduced the directly evoked response by about half. It is concluded that tricaine anesthesia has a pronounced peripheral effect on neuromuscular function and that direct effect(s) on muscle are a major component.

Aminobenzoates↗
PubMed2003

Progressive muscle weakness after high-dose steroids in two children with CIDP.

Corticosteroids and intravenous immunoglobulins belong to the first line of treatment in chronic inflammatory demyelinating polyneuropathy. In patients with a progressive course, plasma exchange and immunomodulatory drugs are added to the regimen. To reduce the side effects of long-term oral prednisolone, high-dose pulsatile intravenous methylprednisolone treatment has been advocated. We report two children with chronic inflammatory demyelinating polyneuropathy who, after high-dose intravenous pulsatile methylprednisolone, experienced a significant clinical deterioration with profound loss of muscle strength. Both patients improved after changing treatment to immunoglobulins in one and cyclosporine combined with immunoglobulins and oral prednisolone in the other.

Child↗
PubMed1996

[A 34-year-old woman with delayed motor milestones, high arched palate, and proximal muscle weakness].

We report a right-handed 34-year-old woman with diffuse muscle atrophy. The patient was a full-term infant of uneventful delivery, however, motor milestones were delayed in that neck control was obtained at 10 months of the age and she started to walk unassisted at 2 years of the age. Mental development was normal. She was unable to run with her mates at her kindergarten and she required a handrail when she walk up the stairs. She could not close her mouth completely at the primary school. She was unable to use a straw as a middle school pupil. Recently, she noted difficulty in raising her head from the supine position, and has become unable to walk a long distance. She was admitted to our hospital in September 17, 1994 when she was 34-year-old. On admission, general physical examination revealed that she looked slender weighing 38 kg with 149.5 cm height. She showed a high arched palate, slight scoliosis, and pes equinus. Otherwise general physical examination was unremarkable. Upon neurologic examination, she was alert and well oriented. Cranial nerves were unremarkable except for bilateral facial atrophy and moderate weakness. Her voice was of nasal quality, and swallowing was slightly difficult. No atrophy was noted in the sternocleidomastoid muscle. She showed waddling gait and positive Gowers' sign. Diffuse muscle atrophy was noted and mild to moderate weakness was presented more in the proximal part in both upper and lower extremities, however, deltoid muscles retained normal power. No ataxia was noted. All the deep tendon reflexes were lost. Sensation was intact. Routine laboratory examination was unremarkable. Serum CK was 56 IU/l. Electromyography revealed myogenic changes in the deltoid, biceps, and quadriceps muscles. A diagnostic biopsy was performed in the left biceps brachii muscle. The patient was discussed in the neurologic CPC, and the chief discussant arrived at the conclusion that the patient had nemaline myopathy. Opinions were divided among nemaline myopathy, central core disease, and congenital fiber type disproportion. Histologic examination of the biopsied specimen revealed marked atrophy of type 1 muscle fibers; many central nuclei were seen in the type 1 fibers. Approximately 70% of the muscle fibers were type 1 fibers. No nemaline rods or central cores were noted. Histologic appearance was consistent with the diagnosis of congenital fiber type disproportion.

Adult↗
PubMedDate not supplied

[Arthroscopic joint debridement for gonarthrosis: influence of degree of chondral damage and muscle weakness on results].

AIM: Purpose of this study was to investigate the correlation between subjective patient discomfort, chondral damage and muscular weakness in cases of gonarthrosis (OA). METHODS: In 22 patients suffering from OA who underwent arthroscopy, the complaints were scored by the Lysholm score. Chondral damage was determined by a special "chondral score". The maximum peak torque was measured pre- and postoperatively (isokinetic test, Cybex 6000 dynamometer). RESULTS: Joint debridement and subsequent postoperative aggressive rehabilitation produced a significant increase in the Lysholm score (from 45.7 to 77.5 points). Subjective complaints correlated significantly with the degree of chondral damage. After treatment, the strength of the extensor muscles increased significantly. The strength of the flexor muscles strength also increased tendentially. However, there was a deficit in muscular strength in comparison to the contralateral leg in all cases. The subjective complaints correlated with the loss of muscle strength at slow angular velocities. CONCLUSIONS: The patients" evaluation with the Lysholm score in combination with an arthroscopic chondral score and the measurement of the isokinetic muscle strength is a suitable method to obtain information about the chances of success for arthroscopic joint debridement in patients suffering from OA. Arthroscopic treatment is an appropriate measure for a short-term reduction of subjective complaints in OA. But it is also useful to reduce muscular deficits.

Adult↗
PubMed1999

Organ-specific autoantibodies with muscle weakness.

The motor unit includes the anterior horn cell, the motor axon and the muscle fibers it innervates, and the neuromuscular junction. Diseases of the motor unit usually present with weakness. Diagnosis of motor unit disorders involves the history, physical examination, electrophysiologic studies of nerve and muscle, and blood testing for creatine kinase, genetic disorders, and autoantibodies. Antibody testing is often useful for the identification of specific immune-mediated motor unit disorders. Identification of these disorders is important because they are often treatable. Antibodies with disease specificity include those directed against autoantigens with and without organ specificity. Several autoantibodies to non-organ-specific antigens are associated with subgroups of immune myopathies. Organ-specific autoantibodies in motor unit disorders with weakness occur in myasthenia gravis, especially with thymoma, a myopathy associated with Waldenstrom's macroglobulinemia, Lambert-Eaton myasthenic syndrome, and multifocal motor neuropathy.

Autoantibodies↗