11 April 2022
Muscle Atrophy Treatments
Muscle atrophy affects millions of people, and moderate and severe forms are associated with significant morbidity and mortality. While physical exercise and electrical stimulation are the only effective treatments for mild to moderate atrophy, drugs may slow the degeneration of muscle and cause serious side effects. Novel interventions are needed to improve muscle physiology and improve the quality of life for people suffering from atrophy. Listed below are some treatments for atrophy. The following article discusses each one in detail.
Disuse atrophy
Immobilization, particularly tenotomy, can induce disuse atrophy of muscle. While AFOs can provide functional immobilization without causing complete immobilization, they may also be associated with disuse atrophy of muscle. MAFOs, on the other hand, restrict movement by preventing complex inversion, abduction, and plantar flexion. Because they restrict movement to only dorsiflexion, MAFOs may contribute to disuse atrophy in patients with neuromuscular deficits.
The process of atrophy is similar to that of bone and nerve damage. While disuse atrophy occurs after prolonged immobilization or after a traumatic injury, it is often less severe and has little long-term effect on the rest of the body. X-rays can reveal the effects of this condition within a few weeks. The findings suggest that muscle atrophy may be caused by alterations in genes regulating bone turnover, PGC-1a and its downstream target genes.
Peroneal muscular atrophy
Pyramidal peroneal muscular atrophy is a rare affliction that has features that distinguish it from other forms of this disease. It has been classified as hereditary motor and sensory neuropathy (HMSN) type V by Dyck. Dyck classified this disease with lower motor neuron involvement as a complication. However, in patients with this disease, peroneal atrophy predominates over spasticity.
The most common type of peroneal muscular atrophy is Charcot-Marie-Tooth disease, a group of inherited neuromuscular diseases characterized by distal muscle weakness. The disorder first appeared in 1886, when the neurologist Howard Henry Tooth described it as a type of neuropathy characterized by a progressive weakness of the lower extremities. The disease is often associated with a foot drop. The early-childhood form of CMT is the fastest-progressing type, with a pronounced disturbance of gait. Rarely, CMT can affect the hands as well.
Charcot-Marie-Tooth disease
Charcot-Marie-Tooth disease is a genetic disorder that affects both the motor and sensory nerves. Both types of nerves help the body feel and communicate, so when one of these nerves is affected, muscle atrophy results. Symptoms typically begin in the feet or legs, but can also develop in the arms and hands. Symptoms usually start in adolescence or early adulthood, and can eventually affect the entire body.
The symptoms of Charcot-Marie-Tooth disease are progressive and often irreversible. This progressive disorder affects the nerves that carry sensory and motor information from the brain back to the muscles. People with CMT typically exhibit muscle weakness over a period of years, and symptoms usually begin in their legs and feet. The condition can also affect the hands, since the nerves in these areas are long.
Neuromuscular blockade
Patients treated with neuromuscular blockade (NMBD) may develop a pronounced loss of strength, weakness, and endurance. These conditions can be related to protein catabolism and decreased cardiovascular function. While a variety of factors can influence NMBD action and onset, the following are common risks associated with NMBDs:
During the acute phase of muscle atrophy in the ICU, UPP activity increases. This is induced by several factors, including increased inflammatory response, increased cytokines, and increased superoxide in tissues. The upregulated ubiquitin gene transcripts increase the hydrolytic activity of the 20S and 26S-proteasome complexes, which lead to extensive degradation of ubiquitin-binding proteins.
Nutrition
If you have a neurological illness, it can be difficult to maintain the muscle mass you need to fight atrophy. Muscle atrophy can be debilitating and family members can become worried about your skinny appearance. However, the good news is that physiologic atrophy is reversible. In many cases, mild activity and nutrition can prevent atrophy and help you build muscles. In some cases, physiotherapy and close consultation with a doctor are required.
Muscle atrophy occurs due to a number of factors. Lack of use of muscles, neurological diseases, and prolonged hospitalization can cause muscles to thin out. A lack of quality nutrition can make this process much more accelerated. However, if you’re looking for a natural cure, there are several nutritional approaches available. Some of them include the Mediterranean, Nordic, and traditional Asian diets. Choosing a diet that meets your specific needs is crucial to your success in fighting atrophy.
Exercise
Among the symptoms of muscle atrophy is a loss of strength and muscle size. Similarly, reduced protein synthesis and increased degradation can also contribute to muscle atrophy. Loss of muscle mass can have detrimental consequences, extending recovery times and making the condition a leading cause of chronic diseases. Fortunately, there is no known cause or cure for muscle atrophy, but exercise is one treatment option. Studies have shown that adherence to a regular exercise routine can improve overall health.
Muscle Atrophy Treatments
Physical activity has several other benefits for those suffering from muscle atrophy, such as reducing the risk of blood clots and avoiding bedsores. It also reduces muscle stiffness and minimizes nerve damage. In addition, it helps prevent onset of muscle atrophy. If diagnosed early enough, physiologic atrophy can be reversed. It takes time for the muscles to rebuild themselves, but if performed regularly, exercise can help prevent muscle atrophy.