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This may cause paralysis at the later stages of the disease. If a muscle is affected by death of its motor neurons, this means that it does not get nourishment. Therefore, the muscle wastes away (atrophy) leading to hardening of the muscle (sclerosis).
The main characteristic of this disorder is the destruction and death of the motor neurons in the brain and spinal cord in which before their destruction they develop inclusions in their structures-the axon and cell bodies that are rich in protein. The proteins are believed to be as a result of a problem in the degeneration of protein and these inclusions have a substance called ubiquitin and this combines with one of the proteins associated with ALS for example TAR DNA binding protein. (Murray, 2006)
As the motor neurons get destroyed in the lateral and anterior parts of the spinal cord, the neurons are replaced by astrocytes that cause sclerosis. The degeneration of the upper motor neurons that is located in the cortex of the brain results in paralysis, increased reflexes and stiffness of the affected muscles.
The degeneration of the motor neurons that is located in the in stem and the horn-like part at the anterior of the spinal cord results in flaccid paralysis, weakness of muscles and atrophy of the muscles, decreased reflexes and decrease in the muscle tone.
The initial symptoms of this disorder are generally, muscle weakness affecting mostly those of the arms and legs, cramping, difficulty in swallowing, problems in speech and breathing and stiffness of the muscle that has been affected. (Murray, 2006) When the clinical manifestation is first noticed in the arms and legs, it is referred to as limb-onset ALS whereas if the symptoms affect the speech first it is called bulbar-onset ALS.
The bulbar symptoms include difficulty in speech, difficulty in swallowing, drooling, atrophy and fasciculation of the tongue. When the upper motor neurons are affected, the disorder is
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