Muscles Involvement in Neurologic Disease - Essay Example

Muscles Involvement in Neurologic Disease Muscle is highly plastic and many changes occur in muscleas a result of neurological disease. Critically evaluate this statement. Introduction Naturally, muscles are elastic, contractile, extensible and excitable. These are four main features of muscles. However, in the neurologic disease, like MS these functions especially excitability are impaired. Studies have identified plasticity of muscles as an important element that explains the neurological impairment in the disease (Compston & Coles, 2008b). MS forms part of neuromuscular disease is a cluster of over twenty diseases whose effects impairs nerves, muscles and synapses between them. Some of these conditions include neuropathy that is most common, characterized by weakness, changes in skin color and numbness. Notably, in MS disease, the muscles loses their elasticity, spasm and rigidity ensue (Nylander & Hafler, 2012). Multiple Sclerosis (MS) is one of the conditions of neurons origin that causes extensive muscles involvement. After extensive research, it was established that the disorder was of one the muscles-involving disease that continue to impair muscles plasticity. Together with other diseases such as Myasthenia gravis, Parkinson, it has been established that muscular involvement in these diseases arises from the neuromuscular connection. Multiple sclerosis refers to a neuron disease that occurs when nerves undergo degeneration resulting in loss of functions. The exact cause of the disease is largely unknown. However, existing studies links it to an autoimmune disorder that cause destruction of nerves (Compston & Coles, 2002, 2008b). In other severe cases, loss of nerves functioning causes permanent disability since nerves cannot be regenerated. This focus will examine existing literature to provide an association of muscles properties and neurological involvement. Muscle is an integral part of the skeletal and even visceral parts of the human body. There are of either skeletal or visceral origin. Irrespective of their types, they are needed for normal body function. More specifically, skeletal muscles are necessary in support and movement and visceral muscles are primary parts of internal organs. Besides, they facilitate tissues and organ varied degree of changes including peristalsis. However, in MS, muscles are significantly impaired depending on their location and severity of the disease. To understand the basis of muscles involvement in MS, it is important to look at the Central Nervous System (CNS) and more specifically structural components of a nerve. One way to understand this is to consider myelin sheath autoimmune destruction. During MS, there is gradual attack of the myelin sheath by the auto-destructive antibodies (Coales, 2000). More specifically, some skeletal muscles will often not contract unless stimulated through a cascade of neurological transmission (Antel, Antel, Caramanos, Arnold, & Kuhlmann, 2012). However, cardiac and smooth (visceral muscles) can contract without this stimulation. Thus, focusing on skeletal muscles action about neurological disease will give clear insight on mechanism of muscles involvement. Many neurological conditions has multiple muscular manifestation including MS, myasthenia gravis. This has been explained using autoimmune destruction of nerve tissues or disturbance in neurotransmitter and subsequent neuromuscular junction (Sherwood, 2010). Consequently, there is reduced sensitivity and loss of muscular functions. Ultimately, the involvement of muscles in neurologic diseases cause disability and gradual permanent loss of muscular functions. Discussion The relationship between muscles and MS disease involves multiple events occurring at neurons. They gradually impair muscles in two ways. Firstly, the effect could be a result of the direct pathological process nerves that causes loss of myelin sheath. Destruction of myelin sheath impairs nerves’ ability to transmit an impulse across neuromuscular junction (Lassmann, 2011). Whichever the case, the disease will manifest in muscles. After long studies, it has been established that MS diseases either causes muscles rigidity, loss of response and spasticity or varying the degree. With increased age, it has been identified as one of the leading causes of paralysis (McDonald et al., 2001). Thus, muscles plasticity is impaired in both cases. The second adverse effect of the disease is a disability. A large proportion of people suffering from this condition gradually causes problems with movement and vision. This has been possible because of the essential role of movement and balancing that primarily executed by synergistic muscular movements. Over 30% who are diagnosed of MS develop significant disability after 20-25 years (Compston & Coles, 2008a). As muscles plasticity is lost, ability to perform daily chores is diminished. Other studies have found that other people can live with this condition for life. More studies have established that with decreasing myelin fat tissue, there is gradual loss of impulses during conduction. As a result, the threshold to elicit muscle response at neuromuscular junction is lost. Therefore, it is plausible to link loss of muscles plasticity to pathology of nerve that cause a subsequent loss of transmission. Besides, MS disease affects both bigger and small muscles, as a result people with this disease have multiple manifestation (Albrecht & Wiesmann, 2006). Apart from evidence of long-term disability, existing studies link MS to loss of plasticity of ocular muscles (Ge, 2006). One of the striking feature is visual changes, mostly described by patients as blurred or hazy. In advance MS, there is an attack on the myelin sheath of optic nerve resulting in formation of inflammation of the nerve. As a result, tissues around the eye starts becoming painful. Some studies state that most people may regain their visual muscles plasticity if intervention is timely, while others are left with permanent eye damage. The decline in the amount of transmitter necessary to conduct an impulse from one cell to the next explains the increase in muscle rigidity and gradual loss of its plasticity. MS is an exemplary example, loss of myelin sheath in the dopamine-containing nerves in the brain resulting in a slow loss of cells excitability. Consequently, muscle plasticity is lost. Lastly, brain structural damages have shown reduced in physical function. Symptoms of Multiple Sclerosis To explain whether muscle plasticity is linked to the neurological diseases, it is important to examine the common clinical manifestations that present. The most common clinical features include muscle weakness, loss of muscular control and rigidity or sometimes muscles flaccidity. More importantly, these are severe symptoms. Other findings include muscles twitching, myalgia and observable loss of muscles tone. Diagnosis relies on imaging studies and sometimes genetic testing is possible inherited neuromuscular conditions (Antel et al., 2012). Notably, symptoms cause loss of plasticity, the change in elasticity and extensibility in disease muscles is a clear manifestation of an extrinsic pathology. Some of the other symptoms that is specific to MS disease include loss of vision and disability. Because of wide distribution of the nerves of CNS in the body, there are varied presentations depending on the location of body affected. Therefore, symptoms varies, some of the common manifestation include fatigue, continence due to urethra and bladder muscles incompetence. Although not common, swallowing and speech problems have been identified as possible involvement of vocal cord muscle destruction. In addition, pain and constipation due to involvement of intestinal muscles. Others include changes in sensation and cognitive impairment. The fundamental basis of these clinical features can be explain based on loss of nerve tissue that supply specific muscle. However, although this condition is incurable, most of these symptoms can be alleviated with medication. There is increasing evidence linking MS due loss of muscle tissue due to disuse. After irreparable damage has been done, patients start presenting with troubled posture and fatigue. Muscles weakness, spasm and numbness are common presentations at the muscles. Depletion of nerves in the CNS causes problems in focusing or remembering. As the muscles continue to undergo damage, there is loss of neurotransmitter efficiency, as a result firing of neurons to elicit a motor movement increases in threshold Langdon, (2011) states that some of these symptoms have been seen in patients aged 20-40. Thus, it has been established that both large muscles and fine muscles undergo changes almost simultaneously. While there has never been exact cause of this neural degeneration, there is growing body of evidence linking vitamin D deficiency with poor immune and skeletal predisposing factors. Others describe MS as an autoimmune destruction of healthy nerves. Irrespective of the cause, this condition has primarily cause impairment of the muscles resulting in multiple defects. Movement and coordination are centrally controlled from the cerebral cortex. Abnormality in the structure or abnormal firing of neurons results in a change in muscles plasticity. Seizure is a good example of abnormal neuron firing and stiffening of the muscles. Hence, it can be concluded that plasticity of the muscles is primarily controlled by the brain. As a result, any imbalance either structural or functional will result in muscles involvement. With existing studies, it is plausible to link muscles involvement in neurologic conditions to the three fundamental findings. More studies need to be done to explore at length relationship with plasticity of the muscles. Conclusion There has been studies suggesting an autoimmune mechanism while others suggest possibility of genetic inheritance. A systematic pattern can be explained by examining the structural changes of a nerve cell during disease and the effect on nerve impulse transmission. A number of studies examined provide a substantial literature background that strongly link muscular involvement in MS as a secondary effect after the primary destruction of the nerve cell (Langdon, 2011). Notably, involvement of eye, intestinal, brain or even esophageal smooth muscles shows gravity of the neurologic extension to the muscles. Polman et al., (2005) argue that some of the neurological conditions are caused by autoimmune conditions. The mechanism of the pathological process goes back to the destruction of the neurons end plates, thus reducing the viability of the neural receptors. Irrespective of the cause of the neural pathology, muscular dysfunction is observed across the conditions. Based on the study of the multiple diseases of neurologic origin, it can be concluded that muscles involvement is linked to three factors. Firstly, the structural destruction of nerve endings receptors binding muscles to another. As a result, there is a loss of stimulation and excitability of the adjacent muscles cells (Graber & Dhib-Jalbut, 2011). An arrest of neural stimulation results in gradual inactivity of the muscle. Autoimmune mechanism of auto-receptor destruction can be explained by this suggestion. Based on the findings in MS, it is plausible to conclude that muscles’ plasticity is highly impaired in neurologic disease because of two reasons. Any disease affecting any part of this connection like MS will have negative effects on the muscles plasticity. The loss off myelin sheath in MS disease results in decrease competence in neural transmission resulting in declined response to a nerve impulse (Fischer et al., 2013). Similarly, to other neurologic diseases, MS is gradual, incurable and causes incapacitation if symptoms are not managed early. Reference List Albrecht, J., & Wiesmann, M. 2006. The human olfactory system. Anatomy and physiology. Der Nervenarzt, 77(8), 931–939. http://doi.org/10.1007/s00115-006-2121-z Antel, J., Antel, S., Caramanos, Z., Arnold, D. L., & Kuhlmann, T. 2012. Primary progressive multiple sclerosis: Part of the MS disease spectrum or separate disease entity? 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