Respiratory muscle training in children and adults with neuromuscular disease.
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ABSTRACT:
SUBMITTER: Silva IS
PROVIDER: S-EPMC6953358 | biostudies-literature | 2019 Sep
REPOSITORIES: biostudies-literature
Publications
Respiratory muscle training in children and adults with neuromuscular disease.
Silva Ivanizia S IS Pedrosa Rafaela R Azevedo Ingrid G IG Forbes Anne-Marie AM Fregonezi Guilherme Af GA Dourado Junior Mário Et ME Lima Suzianne Rh SR Ferreira Gardenia Mh GM
The Cochrane database of systematic reviews 20190905
<h4>Background</h4>Neuromuscular diseases (NMDs) are a heterogeneous group of diseases affecting the anterior horn cell of spinal cord, neuromuscular junction, peripheral nerves and muscles. NMDs cause physical disability usually due to progressive loss of strength in limb muscles, and some NMDs also cause respiratory muscle weakness. Respiratory muscle training (RMT) might be expected to improve respiratory muscle weakness; however, the effects of RMT are still uncertain. This systematic review ...[more]
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Project description:Pompe disease is due to mutations in the gene encoding the lysosomal enzyme acid ?-glucosidase (GAA). Absence of functional GAA typically results in cardiorespiratory failure in the first year; reduced GAA activity is associated with progressive respiratory failure later in life. While skeletal muscle pathology contributes to respiratory insufficiency in Pompe disease, emerging evidence indicates that respiratory neuron dysfunction is also a significant part of dysfunction in motor units. Animal models show profound glycogen accumulation in spinal and medullary respiratory neurons and altered neural activity. Tissues from Pompe patients show central nervous system glycogen accumulation and motoneuron pathology. A neural mechanism raises considerations about the current clinical approach of enzyme replacement since the recombinant protein does not cross the blood-brain-barrier. Indeed, clinical data suggest that enzyme replacement therapy delays symptom progression, but many patients eventually require ventilatory assistance, especially during sleep. We propose that treatments which restore GAA activity to respiratory muscles, neurons and networks will be required to fully correct ventilatory insufficiency in Pompe disease.
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