Muscle Weaknesses And Paralysis

Most people do not expect to become paralyzed during the course of their lives. Barring injury to the nervous system or debilitating disease, one does not expect to lose motor function. In spite of these expectations, people of all races, sexes, ages, and classes can be afflicted with a debilitating syndrome that can lead to difficulty in walking or even to temporary paralysis in the most severe cases. This syndrome is known commonly as Guillain-Barre Syndrome, or GBS.

Multiple Sclerosis and Guillain-Barré Syndrome are two autoimmune disorders of the nervous system that occur when the myelin sheath surrounding the axons of a nerve degenerate. Multiple sclerosis (MS) affects the central nervous system while Guillain-Barré Syndrome (GBS) involves the peripheral nervous system.1,2 MS is a gradually regressing disease that usually occurs in one of four ways. The first is relapsing-remitting MS (RRMS) and is the most common. Patients typically experience relapses where the symptoms are aggravated and enhanced followed by episodes of remissions during which the symptoms cease or calm down. 3 The second type is called secondary-progressive MS (SPMS). This type mimics RRMS but undergoes a steadier decline that may or may not include relapses3. The third type is primary-progressive MS (PPMS) where the disease progresses at a more regular rate from onset. PPMS, however, may speed up, slow down, or even plateau for a bit, but no remissions are present.3 Lastly, progressive-relapsing MS (PRMS), the least common type, presents similarly to PPMS in that the decline is steady, but this type of MS has exacerbations that the patient may or may not recover from.3 Unlike MS, Guillain-Barré does not present in types and characteristically attacks more rapidly.2 It is a poorly understood disease, however, research has shown that it is generally preceded by a bacterial or viral infection.4

This fact is substantiated by the progressive disease Amyotrophic Lateral Sclerosis. This progressive neurodegenerative disease disrupts nerve cells' ability to function (Amyotrophic Lateral Sclerosis). It is considered a terminal disease because those diagnosed with the disease die normally within three to four years. Nerve cells commonly referred to as motor neurons act as modes of communication that convey signals to the concerning body part. These messages sent from the brain are the catalyst for all the body’s movement and functions. According to the ASL association, the brain integrates, coordinates, and processes voluntary and involuntary actions (1). The brain works effectively to assure that all processes are performed correctly. Oppositely, those afflicted with ASL are unable to coordinate the body necessary components. This results in limited mobility which results in atrophy.

Multiple sclerosis is an autoimmune disease that majorly affects the brainand the spinal cord (A.D.A.M. Medical Encyclopedia, 1). The disease affects the central nervous system and thus causes limitations of individuals to carry out various activities. In multiple sclerosis, the myelin sheath that covers nerve cell axon is destroyed causing inflammation (MediResource Inc., 1). Destructionof the membrane leads to slowed conveyance of signals from the spinal cord to the brain, which as a result leads to reduced response to different stimuli. Inflammation of the nerve occurs mostly when the immune cells from the body attack the nervous system. The inflammation is not only limited to the spinal cord, but sometimes extends to

Multiple sclerosis affects various parts of the body, mainly the brain and the spinal cord. When the myelin sheath is damaged by the immune system, nerve signals have difficulty transmitting. This creates various problems such as numbness, loss of and problems with vision, loss of memory, dizziness, clumsiness. Because of nerve signals failing to transmit properly, many complications arise in relation to simple daily tasks. From exercising to eating, assistance is commonly needed by those who are affected by MS.

eyes, or difficulty getting your legs to walk, or holding on to a wall while ambulating due to severe major cramping and muscle stiffness, these are the real expressions of Multiple Sclerosis. These neurological symptoms were first identified in the early 14th and 15th centuries. The immune system attacks the myelin of the brain & spinal cord causing a cessation or misinterpretation of communication with the rest of the body. Due to this destruction or damage to the myelin, scar tissue forms and there central nervous system cannot communicate with the body effectively. This is the mechanics of Multiple Sclerosis, a disease that affects many people across the globe.

The myelin sheath is where the nerve axons serve as an electrical insulator that speeds up nerve impulses to muscles and other effectors. The damage of the myelin sheath is caused by inflammation of the brain, and may have significant damages to other areas as well. Damaged areas undergo scarring or plaques. Plaques may be found in different areas of the brain, which include: optic nerves, spinal cord, cerebellum, brainstem, and cerebral area of the brain. Researchers have found evidence of damage to the gray matter of the brain as well. The symptoms of MS are related to the interruption of sending signals between the neurons. Damage caused by axons will cause an irreversible disability that will continue to debilitate the individual for their life. As a result of MS, people with this disease may lose the ability to walk. The myelin sheath debilitates the person to walk and results in having it for their rest of their life.

Guillain-Barre syndrome (GBS) is classified as an acute inflammatory demyelinating polyneuropathy (AIDP), an autoimmune disease that causes damage to and attacks the peripheral nervous system, and is usually caused by an acute infectious process (Bussmann, Garssen, van Doorn, & Stam, 2007). Hiraga et al. (2005) characterise GBS as an ascending paralysis beginning with weakness of the lower leg limbs spreading to the upper body limbs through into the abdomen and in severe cases into the face. Although to date there is no cure for GBS, there are several treatments that can relieve symptoms and minimise the duration of the illness. The usual process of recovery for GBS is through high-dose immunoglobulin therapy or Plasmapheresis, followed by

Two other characteristics are involved in the disease process: inflammation and the formation of lesions or plaques in the central nervous system – or CNS (Mayo Clinic Staff, 2014). Lesions are formed when oligodendrocytes – myelin-building cells – are lost causing the myelin sheath to thin or even completely breakdown leaving the nerve axon exposed and unable to send effective signals to your muscles (Huether and McCance, 2008). The oligodendrocytes attempt to remyelinate the axons but with multiple attacks, the

Guillain-Barre Syndrome (GBS) is a disorder where your own immune system starts to attack part of the nervous system, mainly the peripheral nervous system. The peripheral nervous system is a very important system in the body it is what contains all the nerves that are not directly connected to the brain and spinal cord. The main function of the peripheral nervous system is to connect the central nervous system to the rest of the body, such as the organs and limbs. Beginning signs that you may have Guillain-Barre Syndrome is that of noticing varying degrees of tingling and weakness in the legs, most people throw this sensation off for restless leg syndrome so they never go to get diagnosed for the disease. Guillain-Barre syndrome can affect

Hyperkalemic Periodic Paralysis is a disease that is found in horse that leads to random muscle spasms as well as gradual muscle weakness. The disease is caused by mutations in the SCN4A gene, specifically the gene carries what is called a NaV1.4-R669H variant (Fan 2017). It is a dominant allele meaning that if the parent carries it than the offspring has a fifty percent chance of contracting it themselves. The SCN4A gene codes for the sodium channel NaV1.4 within the muscles (Wu 2011).

Guillain-Barré Syndrome (GBS) is an immune mediated peripheral neuropathy primarily characterized by rapidly evolving symmetrical limb weakness1. The weakness can be variable, from minimal lower extremity weakness to total paralysis of all extremities and trunk. Symptoms become more severe until they reach maximum expression, called the nadir; a plateau phase of 2-4 weeks follows, & recovers completely within 1 month after the onset. But in rare cases there is a gradual resolution of the paralysis that can last 1-2 years & the patient recovers within a period of 6 months to 2 yrs1.The patient being reported in this case study is a 40 year old male diagnosed with GBS and reached a plateau phase within a month & recovery is not complete even

Our muscle mass and bone atrophies start after every decade as we age pass 30. People who have been involved into physical activities since when they were young doesn’t suffer from that excessive muscle and bone tissue loss. Strength training in particular prevent muscle/bone loss and helps in hypertrophy. For older population muscle and bone atrophies bring many challenges particularly in maintaining right posture and range of movement. That is why often times we have seen seniors with slouched back and frozen shoulders. The unfit seniors face many difficulties in performing routine task such as climbing on stairs. Stand for prolong period or lifting heavy objects.

The manifestations of ALS are caused by the location of motor neuron death. When upper motor neurons die, the symptoms include problems controlling fine movements, spasms, dysphagia, dysphonia and dysarthria (Porth & Matfin, 2009). “Manifestations of lower motor neuron destruction include fasciculations, weakness, muscle atrophy, and hyporeflexia” (Porth & Matfin, 2009, p. 1284). Patients with early signs of ALS usually complain of feeling weak on one side, which is due to the slowing of electrical impulses to that group of muscles (Ignatavicius & Workman, 2010). Since the impulses are slowed, they are not receiving adequate electrical stimulation to move and the person feels weak. As the disease progresses, all the motor neurons die and are not regenerated so, the patient is left paralyzed, losing the ability to speak, swallow and breathe (Ignatavicius & Workman, 2010).

Regardless of which occur first, affected individuals will generally experience most of the symptoms as the disease progresses. Specifically, symptoms that include difficulty swallowing, moving, forming words, tight muscles, spasticity, and/or exaggerated reflexes occur when the upper motor neurons have been damaged. When lower motor neurons are damaged, symptoms such as muscle weakness, atrophy, cramping, and twitching will occur. In some cases, a few of the muscle neurons that