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Types There are different types of muscular dystrophy, including the following: The most common form of the illness. Symptoms normally start before a child's third birthday; they are generally wheelchair-bound by 12 years and die of respiratory failure by their early-to-mid-twenties.
Similar symptoms to Duchenne but with a later onset and slower progression; death usually occurs in the mid-forties. The myotonic form is the most common adult-onset form. It is characterized by an inability to relax a muscle once it has contracted. The muscles of the face and neck are often affected first. Symptoms also include cataracts , sleepiness, and arrhythmia. This type can be obvious from birth or before the age of 2 years.
It affects girls and boys. Some forms progress slowly whereas others can move swiftly and cause significant impairment.
All about muscular dystrophy
Onset can be at almost any age but is most commonly seen during teenage years. The muscular weakness often begins in the face and shoulders.
People with FSHD may sleep with their eyes slightly open and have trouble fully closing their eyelids. When an individual with FSHD raises their arms, their shoulder blades protrude like wings. This variant begins in childhood or teenage years and first effects the shoulder and hip muscles. Individuals with the limb-girdle muscular dystrophy might have trouble raising the front part of the foot, making tripping a common problem. Onset is between the ages of 40 and 70 years.
Eyelids, throat, and face are first affected, followed by the shoulder and pelvis. Causes Muscular dystrophy is caused by mutations on the X chromosome.
Each version of muscular dystrophy is due to a different set of mutations, but all prevent the body from producing dystrophin. Dystrophin is a protein essential for building and repairing muscles. Duchenne muscular dystrophy is caused by specific mutations in the gene that encodes the cytoskeletal protein dystrophin. Dystrophin makes up just 0.
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Dystrophin is part of an incredibly complex group of proteins that allow muscles to work correctly. The protein helps anchor various components within muscle cells together and links them all to the sarcolemma - the outer membrane.
If dystrophin is absent or deformed, this process does not work correctly, and disruptions occur in the outer membrane. This weakens the muscles and can also actively damage the muscle cells themselves.
In Duchenne muscular dystrophy, dystrophin is almost totally absent; the less dystrophin that is produced, the worse the symptoms and etiology of the disease. In Becker muscular dystrophy, there is a reduction in the amount or size of the dystrophin protein.
The gene coding for dystrophin is the largest known gene in humans. More than 1, mutations in this gene have been identified in Duchenne and Becker muscular dystrophy. Diagnosis There are a variety of techniques used to definitively diagnose muscular dystrophy: The genetic mutations involved in muscular dystrophy are well known and can be used to make a diagnosis.
Damaged muscles produce creatine kinase CK. Elevated levels of CK in the absence of other types of muscle damage could suggest muscular dystrophy. As genetic mutations are known to occur in muscular dystrophy, these changes can be screened for. Electrocardiography and echocardiograms can detect changes in the musculature of the heart. This is especially useful for the diagnosis of myotonic muscular dystrophy. Checking lung function can give additional evidence.
A needle is placed into the muscle to measure the electrical activity. The results can show signs of muscle disease. Removing a portion of muscle and examining it under a microscope can show the tell-tale signs of muscular dystrophy. Outlook The outlook will depend on the type of muscular dystrophy and how severe the symptoms are. Duchenne muscular dystrophy can lead to life-threatening complications, such as breathing difficulties and heart problems.
In the past, people with this condition did not usually survive beyond their 20s, but progress is improving the outlook. Currently, the average life expectancy for people with Duchenne is 27 years , and it may improve in time, as treatment progresses.
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A person with muscular dystrophy is likely to need lifelong assistance. Current research A great deal is known about the mechanisms of muscular dystrophy, both muscular and genetic, and although a full cure may be some distance away, there are avenues of research that draw ever closer to one.
Gene replacement therapy Gene therapy is just one strand of research into treating muscular dystrophy. Because the specific gene involved in muscular dystrophy has been found, a replacement gene that could create the missing dystrophin protein is a sensible consideration. There are complicated problems with this approach, including the potential of the immune system to repel a new protein and the large size of the dystrophin gene needing to be replaced. There are also difficulties in targeting viral vectors directly to the skeletal muscle.
Another approach targets utrophin production. Utrophin is a protein similar to dystrophin that is not affected by muscular dystrophy. If utrophin production could be upregulated, the disease might be halted or slowed. Altering protein production If the dystrophin gene is being read by protein synthesis machinery and it reaches a mutation, it stops and does not complete the protein.
Drugs are being trialed that cause the protein-making equipment to skip the mutated content and still continue to create dystrophin. Drugs to delay muscle wasting Rather than target the genes behind muscular dystrophy, some researchers are attempting to slow the inevitable muscle wasting. Muscles, in standard circumstances, can repair themselves. Research into controlling or increasing these repairs could show some benefits for people with muscular dystrophy.
Stem cell research Researchers are looking at the possibility of inserting muscle stem cells capable of producing the lacking dystrophin protein.
Current projects are looking at the most useful type of cells to use and ways in which they could be delivered to skeletal muscle. Myoblast transplantation During the early stages of muscular dystrophy, myoblasts also called satellite cells repair and replace faulty muscle fibers. As the myoblasts become exhausted, the muscles are slowly turned into connective tissue. Some studies have attempted to insert modified myoblast cells into muscles to take over from the exhausted natural myoblasts.