Amyotrophic Lateral Sclerosis Essay

C. Strictly speaking, ALS involves degeneration and death of both upper and lower motor neurons. While most patients have clear loss of both types of motor neurons, some patients have greater loss of upper motor neurons, while other patients have greater loss of lower motor. These differences do not change the diagnosis. In these circumstances, the more general term ‘motor neuron disease’ is appropriate (MDA).

ALS (Amyotrophic Lateral Sclerosis) or Lou Gehrig’s Disease is a classified as a degenerative neurological disorder that inhibits motor neurons in the spinal cord and brain to function properly. This disease eventually results in paralysis and imminent death over a period of time. ALS patients have anywhere from a few months, to a couple years to live after diagnosis since their nervous systems are slowly destroyed, rendering the body useless, and sustaining life impossible.

Amyotrophic Lateral Sclerosis (ALS) is a terminal disease, also known as Motor Neurons Disease, Charchot Disease and Lou Gehrig disease. ALS destroys the Central Nervous System (CNS) and causes damage to the upper and lower motor neurons in the brain. Signs and symptoms are characterized as: muscles weakness, muscle atrophy, twitching and reduced muscle reflexes. Eventually the patient will become paralyzed and rely on a tracheostomy and ventilator for breathing (ALS Association [ALSA], 2010).

Amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig’s disease, is a terminal disease that degenerates the nerves in the brain and spinal cord. Motor neurons run from the brain, through the spinal cord, and into the muscles of person; this is what allows a person to have control over voluntary movement. When an individual is diagnosed with ALS, their motor neurons begin to degenerate, thus eradicating their ability to walk, eat, and eventually breathe.

There are 20,000 new cases of ALS diagnosed each year in the United States. This yields an incidence of 3 per 100,000 (Brown, 2006). There is no known cause for ALS in 95% of patients; however, 5% have an identifiable genetic mutation (Elman, 2016). The disease can present in individuals less than 30 years of age, but peaks between 40 and 60 years of age. Before the age of 65, more diagnoses are made in men; after the age of 65, gender incidence is equal. There is no clear-cut ethnic or racial predisposition in ALS (Ricks, 2016). The lifespan is approximately 3-4 years after diagnosis. However, in 10 % of

It's a brave question because the answers are not very pleasant." When an individual is diagnosed with ALS, they begin a totally new way of life. Surprising, in many cases it can often be difficult to diagnose someone with Amyotrophic Lateral Sclerosis. However, with a history of their problems and a few other tools, it is possible. One of the most common ways to diagnose someone with Amyotrophic Lateral Sclerosis is by looking at their complications. Some of the most common early signs of ALS are a patient's legs may seem to be heavier than normal or

ALS, better known as Amyotrophic Lateral Sclerosis, is considered as a complex genetic disorder, in which multiple hereditary and environmental factors combine to cause this disease. This is seen as an illness of parts of the nervous system that control voluntary muscle movement. In ALS, the motor neurons (nerve cells that control muscle cells) are gradually lost. When these motor neurons turn out to be lost, the muscles they control become weak and ultimately nonfunctional. We see that “amyotrophic” is rooted in Greek origin meaning without nourishment to muscles and refers to the loss of signals nerve cells normally send to muscle cells. “Lateral” simply means to the side and refers to the location of the damage in the spinal cord. “Sclerosis” means hardened and refers to the toughened nature of the spinal cord in advanced ALS. This progressive neurodegenerative disease, that was first discovered 150 years ago, is associated with a life expectancy of approximately three years after symptom onset. In the United States, ALS is also known as Lou Gherig’s Disease, named after the Yankees Baseball player who passed away because of it in 1941. In the United Kingdom and other parts of the world, it’s often referred to as motor neuron disease in reference to the cells that are lost in the disorder (ALS Association, 2015).

There has been recent support for exercising those diagnosed with ALS, but a substantial amount of the research available on this subject has been performed on mice. This has made it increasingly difficult to justify these same treatment guidelines on humans. However, these research studies that have been completed in recent years have shown exercise to be an intervention that can help improve function, slow disease progression, and lessen caregiver burden. For example, aquatic therapy has been found to significantly delay spinal motor neuron death in mice with ALS, as well as preserve astrocyte and oligodendrocyte populations in the spinal cord in a study published in 2009 (cite). In 2003, research demonstrated that a lifetime of vigorous exercise did not promote the onset and/or progression of motor degeneration in mice, revealing the running group of mice demonstrated a non-significant 6-day improvement in survival, compared with the sedentary group, and a 4-day improvement when compared to the control (cite). Lastly, in 2004 a study revealed that exercise delayed the onset of disease in female but not in male hSOD1 mice. Also, exercise delayed the total survival time in female high-copy hSOD1 mice. Sedentary female hSOD1 mice showed more frequently irregular estrous cycles suggesting a higher estrogen exposure

Amyotrophic Lateral Sclerosis is a progressive neurodegenerative disease that affects nerve cells in the brain and the spinal cord. ALS causes muscle weakness and impacts physical functions this occurs in the nervous system. In the nervous system motor neurons of the body are being affected. Usually, ALS causes weakness and paralysis in the muscles. The muscles slowly waste away and a person’s legs and arms become much weaker. In some cases there may be muscle spasms, weight loss, and difficulty in breathing, eating, and swallowing. The mind does not get affected and there is no loss of sensation, or sense of touch during ALS. The average for a person with ALS is about two to five years from the time diagnosis. In some cases people can live with the disease for five years and more. ALS is mostly being develop between the ages of 40 and 70. Athletes usually get diagnosed between 30 and 34. It shows that athletes have had multiple head trauma and they also have abnormal

ALS or Amyotrophic Lateral Sclerosis is a neurodegenerative disease that causes muscle weakness, fatigue, and overall respiratory failure. It can also cause trouble breathing and swallowing.

Taking a closer look at the cerebrum, allows us to have a better understanding of the dying-forward cascade and its important role in initiating disease onset (Thomsen, et al., 2014). The outer layer of this complex organ composed of gray matter is the cerebral cortex, region where the corticospinal neurons related to ALS are located. These upper motor neurons responsible for collecting, integrating, translating, and transferring information to the spinal cord reside in layer 5 of the motor cortex (Thomsen, et al., 2014), and are the most vulnerable to be injured by excitotoxicity initiating an anterograde degeneration. In general, ALS research has devoted less attention to the UMN pathology primarily focusing on the LMN connectivity with the neuromuscular junction (NMJ) (Thomsen, et al., 2014). In spite of this remark, recent studies continue to use spinal cord neurons from transgenic SOD1 mice but their priority has switched to the UMN behavior. On a study using mutant SOD1G39A rats, (Thomsen, et al., 2014) wanted to establish whether the upper motor neuron might still play a critical role in disease progression by knocking down mutant SOD1expression in only the motor cortex. As a consequence of this assay, it was shown for the first time that suppression at the top of the motor neuron pathway results in significant delay in ALS disease onset. Thus, further highlighting the importance of the upper motor neurons in ALS (Thomsen, et al., 2014).

A patient with amyotrophic lateral sclerosis (ALS) would be able to be diagnosed from a patient’s history and a physical examination. Although, the symptoms for this disease might not appear until the age of the 30 with the onset of age 55. A patient with ALS will experience muscle weakness, asymmetric involvement of muscles, decrease of body movements, flaccid and spastic paralysis, and not having control of autonomic, sensory or mental effects.

Amyotrophic Lateral Sclerosis comes from the greek language. ‘A’ means no, ‘myo’ means muscle, and ‘trophic’ means nourishment, all together it means no muscle nourishment. Lateral is talking about around the spinal cord, where it gets scarred and hardens, sclerosis. There are two types of ALS; sporadic and familial. Sporadic is the most common form in the US, 90%-95% of all cases. Familial ALS (FALS) is inherited from people’s parents. In these kinds of families, there is a 50% chance that the offspring will get these gene and may develop

ALS is named for its underlying pathophysiology, which is “amyotrophy” referring to the atrophy of muscles fibers, which denervated as their corresponding anterior horn cells degenerate. “Lateral sclerosis” refers to the changes seen in lateral columns of the spinal cord as upper motor neuron axons in these areas degenerate and are replaced by fibrous astrocytes. ALS affects motor neurons at two or more levels of the motor neuron network supplying multiple regions of the body and as a consequence, the communication between the neurons and muscle is lost, promoting progressive muscle weakening. That is, ALS affects lower motor neurons that reside in the anterior horn of the spinal cord and in the brain stem, corticospinal upper motor neuron

A distinctive characteristic of ALS is that although the motor neurons die, the brain, cognitive functions and sensory neurons stay intact (Porth & Matfin, 2009). This makes the disease especially devastating because patients become trapped inside their dying body, with a fully alert mind, but are unable to move. It is not known what causes the exact death of the motor neurons in the body, but “five percent to 10% of cases are familial; the others are believed to be sporadic” (Porth & Matfin, 2009, p.