Amyotrophic Lateral Sclerosis Physical Therapy Interventions: An Attempt to Limit Debilitating Symptoms

 Amyotrophic Lateral Sclerosis Physical Therapy Interventions: An Attempt to Limit Debilitating Symptoms.The participant will be able to accurately describe the pathophysiology of ALS.The participant will be able to differentiate between at least two major types and subtypes of ALS.The participant will be able to correctly describe at least three common impairments that are a result of ALS.The participant will be able to independently identify at least three specific physical therapy treatment interventions used to alleviate or dissipate symptoms depending on disease progression.Background of ALS HistoryJean-Martin Charcot is a French neurologist, but he was trained as a pathologist. He is known as the father of neurology. In his findings, he and his colleagues were able to discover lesions in 2 distinct places. The first place was the lateral column of the spinal cord and the outcomes presented as progressive paralysis, contractures, but no atrophy. Then they found lesions in the anterior horn of the spinal cord and the outcomes were paralysis, no contracture, but atrophy. ALS was termed in 1874 when Dr. Charcot's lectures were compiled as Oeuvres Completes. However, in some parts of the world, ALS is still termed Charcot's Disease. It become very commonplace to call ALS after a famous baseball player named Lou Gehrig. He was the first baseman for the New York Yankees from 1923 to 1939. He was forced to retire in 1939 after being diagnosed with ALS. He died 2 years later. I want you to remember this timing of 2 years because it is going to become significant after we talk about the different ALS-related diagnoses. Defining ALSWhen we define ALS, it is easy to look at the parts of the words and see what they mean. “A “means without. “Myo” is pertaining to muscle. “Trophic” pertains to growth and nourishment of structures by efferent innervation. This is a disease process of motor neurons, which provides efferent innervation. “Lateral” means pertaining to the side and “sclerosis” is hardening of nervous tissue due to degeneration. Overall, ALS is primarily considered a disease of the central nervous system. The central nervous system is everything pertaining to the brain and the spinal cord. What you see is progressive weakness and/or paresis leading to death in a few years from respiratory compromise. There are people out there who have diagnoses of ALS and have lived 5 to 10 years, but they have a different version of the disease that is in a category now known as ALS-related motor neuron diseases.EtiologyIt has been a very long time since Jean-Martin Charcot determined what he called was ALS, but due to different and updated imaging and genetic studies, the etiology of ALS is determined by the pathophysiology and the associated clinical classifications. Now you are going to see a broad spectrum of ALS-related diseases, but the true ALS as we know it, will have a point of death within 1 to 2 years. Pathophysiological MechanismsALS is a multi-system disease process. It has various pathophysiologic determinates of origin. When we look at the pathophysiology, due to our new genetic and imaging studies, there are 6 ways the origins of ALS can come about. I am going to give you the definitions of them, but we are not going to go through the process of how the etiology comes about. We are not pathologists, but we need to know what they are so we can better explain it to our patients. First.  The first is oxidative stress. Oxidative stress simply means that the motor neuron cells are going to have impaired performance because there are too many oxygen molecules in them. Second.  The second is mitochondrial damage. We all know that the mitochondria is the energy factory. It provides the energy needed for cells to survive and it produces about 90% of that energy. When there is mitochondrial damage, your cells do not get the energy needed to properly function and that contributes to one of the pathophysiological mechanisms seen in ALS. Third.  The third is protein accumulation. We have these various proteins that our cells need to operate.   The first being superoxide dismutase 1 and when there is a shape change or, for a better term, a mutation, in SOD1, it can contribute to motor neuron death. They have also found a mutation of the protein TDP-43 in cases of ALS. When you have an accumulation of these proteins in a mutant form, it contributes to the pathological processes seen in ALS. Forth.  The next is cytoskeletal interruption. Let’s review of the motor neuron.  Figure 1 depicts a nerve cell.  The center of the blue is the cell body. This is where you would find the mitochondria and it is known as the perikaryon. It's like the brain of the motor neuron. Then the long blue stem is the axon. All the impulses travel down the axon to your effector cell, which is the muscle. The impulses travel along the myelin sheath in the nodes of Ranvier. Inside this longitudinal structure (axon) you have a skeleton.  A mutation of profilin, PFN1, which is a gene needed for the growth and development of that cytoskeleton can cause cytoskeletal interruption.  When you do not have that cytoskeleton, the structure loses its strength and the ability to transmit information is lost.  A tree can grow tall and strong with its external bark. When you lose that bark, the tree starts to bend and it cannot grow and produce leaves and fruit. The same thing happens with this axon. It cannot send the necessary impulses and the information to the muscle. When there is a mutation of profilin, this gene is unable to participate in the growth and the development of the cytoskeleton of the nerve axons. Figure 1 Nerve Cell Fifth.  The fifth is glutamate and neuronal toxicity. Glutamate is an excitatory neurotransmitter. It is used in learning and in memory. In the central nervous system, it causes a release of calcium. When you have high levels of glutamate, it causes nerve cells to die. This glutamate toxicity causes calcium to stay in the cell. High...