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Diabetes
Published in Sally Robinson, Priorities for Health Promotion and Public Health, 2021
Motor nerves are those that control movement. When these are damaged, muscles are used less and become weak. Muscle weakness leads to falls or difficulties with tasks such as fastening a buttonmuscle wastingmuscle twitches and cramps
Inherited Myopathic Diseases
Published in Maher Kurdi, Neuromuscular Pathology Made Easy, 2021
In summary, inherited myopathic diseases are characterized pathologically with structural myofibrillar defect, abnormality, or deposition. It should be suspected in early or adult-onset patients presenting with muscle weakness of variable distribution and severity. The gold standard method of diagnosis is muscle biopsy followed by genetic analysis. Genetic counseling of the first-relative degree of the family is important once the mutant gene is newly identified in the patient.
Carnitine transporter deficiency
Published in William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop, Atlas of Inherited Metabolic Diseases, 2020
William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop
Cardiomyopathy and failure respond dramatically to treatment [9, 10] and early therapy with carnitine has been reported [49] to prevent cardiomyopathy. Heart size is reduced to normal within months. Doses have ranged from 50 to 150 mg/kg p.o. [40]. Doses as high as 400 mg/kg have been recommended [15]. Intestinal tolerance often mandates lower dosage. Skeletal muscle weakness improved, although mild proximal muscle weakness has occasionally persisted. However, muscle concentrations of carnitine were documented to increase only slightly to 22–80 mmol/g; control levels are 2500–3500 mmol/g. These observations suggested that muscle oxidation of fat and muscle function may be unaffected until the intracellular muscle concentration of carnitine falls below 30–50 mmol/L or 2–4 percent of normal. Biopsied muscle revealed a decrease of stored lipid with treatment, but not a disappearance [1].
Treatment considerations in myasthenia gravis for the pregnant patient
Published in Expert Review of Neurotherapeutics, 2023
Myasthenia gravis (MG) is an autoimmune disease where antibodies against the acetylcholine receptor (AChR) in the postsynaptic membrane at the neuromuscular junction cause the typical muscle weakness [1,2]. More rarely, pathogenic antibodies are instead directed against muscle-specific kinase (MuSK) or lipoprotein-related protein 4 (LRP4) antigens functionally linked to AChR in the membrane. The muscle weakness can be generalized or localized. It occurs most frequently in extraocular muscles with diplopia and ptosis as troublesome symptoms. Weakness in swallowing and speech muscles as well as in facial muscles is common. Neck, shoulder, and arm muscles have frequently some weakness, whereas leg muscles are rarely affected [3]. Respiratory muscle weakness represents the major threat of MG, and myasthenic crisis with the need of ventilatory support can occur, especially during respiratory infections. Fluctuations during the day and over time are typical for MG. Repetitive and prolonged muscle use increases or precipitates the weakness.
Comparison of sports skills movement training to lower limb strength training for independently ambulatory children with cerebral palsy: a randomised feasibility trial
Published in Disability and Rehabilitation, 2022
Alicia J. Hilderley, Darcy Fehlings, Joyce L. Chen, F. Virginia Wright
CP is caused by damage to the developing brain, which negatively affects gross motor skill acquisition, performance, and PA participation [2,3]. Muscle weakness is a key impairment associated with functional limitations, thus strength-based lower limb training has become a central focus of interventions to improve gross motor function [4]. Strengthening can lead to improved movement outcomes specific to muscles trained [5]. Yet isolated strength gains may not be long-term, and carryover to PA behaviour and performance of functional activities may be temporary [6], prompting concern about the overall utility of this intervention approach [7,8] especially for children who have a higher functional level [9]. Moreover, prioritising impairment-focused goals targeting muscle weakness is not well-aligned with developing and improving meaningful activity-focused advanced gross motor skills that are likely the more salient outcomes to children and parents [10].
Growth differentiation factor-15 as an emerging biomarker for identifying myositis
Published in Expert Review of Clinical Immunology, 2022
IBM patients are usually above the age of 50 years, and suffer from a slow progressive, asymmetrical weakness of the upper and lower limbs. The quadriceps muscle weakness leads to difficulties to rise from a chair or climb stairs, and frequent falls. Finger flexion is also typically involved. Muscle weakness may thus lead to loss of functions and an impairment in activities of daily living. An important clinical feature in many IBM patients is dysphagia, which can even be the initial presenting symptom and may be severe, resulting in aspiration. IBM’s myopathologic characteristics include invasion of non-necrotic muscle fibers by auto-aggressive cytotoxic T-cells and macrophages, with inflammation building up mostly at endomysial sites. Muscle fibers additionally develop degenerative changes, with rimmed vacuoles and inclusions containing aggregates of ectopic proteins [18]. Presence of autoantibodies direct against the cytosolic 5ʹ-nucleotidase 1A (NT5c1A) is highly specific for IBM [19]. There is no standard cure for IBM and the disorder generally does not respond to conventional immunosuppressive treatment. Many immunomodulating drugs have been tested for IBM, but so far no breakthrough has been achieved. A combination of medication and rehabilitation therapy can be beneficial for certain individuals.