Pathways Free Essay
Considerable age is associated with serious neurocognitive and neurodegenerative diseases that extremely complicate and even hamper normal living and functioning. Parkinson’s disease is one of the most common severe and disabling disorders among the elderly. Therefore, sufficient investigation into its pathophysiology, clinical manifestations, and involved therapies can be beneficial for the aging population.
Parkinson’s disease is a severe, incurable neurodegenerative disorder that is common among the aged population. It is primarily accompanied “by systemic non-motor and neurologic symptoms” (McCance & Huether, 2014). Its gradual progression can considerably impair the cognitive and behavioral functions of an individual. Neurologists emphasize that Parkinson’s disease is an extremely acute and incurable disease of the central nervous system that involves serious damage to the basal ganglia and substantia nigra. The disease progression is associated with deficient production of the specific neurotransmitter dopamine that is responsible for passing signals on to the neurons. Such deficiency considerably affects neural connections between the brain divisions and entails nerve cell death that, consequently, impairs normal movement and coordination. Furthermore, other researchers specify that imbalanced neurotransmitter activity occurs due to insufficient dopamine release and the increased level of acetylcholine. Some medical experts indicate that “the presence of Lewy bodies and Lewy neurites” is typical of the disorder (Hauser, 2017).
Parkinson’s disease is inherent in the aging population, particularly prevalent among males rather than females. Despite the ongoing research, the exact cause that triggers this degenerative disorder remains unidentified. However, health care specialists accentuate that the aging process, essential head injuries, unfavorable environmental factors, as well as excessive exposure to detrimental toxins, chemicals, and substances are the primary risk factors for inducing the given abnormality. Moreover, genetics ultimately contribute to Parkinson’s disease etymology. Significant health decline associated with Parkinson’s disease can preclude normal social interaction that, consequently, accelerate the disease progression and aggravate the symptoms specific to the disorder under review.
Such clinical manifestations as hyposmia, increased tiredness, sleep disturbances, apathy, depression, constipation, and urogenital impairments can occur at the outset of the disorder that eventually only aggravate the mental state of the individual. In the early stages, people affected by the affliction in question can also suffer from “autonomic dysfunction, dementia with or without psychosis” (McCance & Huether, 2014). The advanced stages of Parkinson’s disease involve resting tremor, muscular rigidity, “postural instability, bradykinesia,” hypokinesia, “Parkinsonian gait,” and other autonomic and neuroendocrine symptoms (Heyn, 2016). The variety and multitude of the represented clinical manifestations indicate the extent of the abnormalities associated with Parkinson’s disorder. Thus, this neurodegenerative disorder significantly deteriorates the physical health and intellectual capacities of the affected people.
The given degenerative disorder belongs to a group of incurable diseases despite multiple research and surveys. Neurologists widely prescribe levodopa for balancing neurotransmitter activity in the brain, in other words, increasing dopamine and reducing acetylcholine levels. However, it is only effective in relieving symptoms specific to Parkinson’s disease but cannot inhibit its progression. Moreover, levodopa is associated with several adverse effects, such as motor “fluctuations and dyskinesia” (McCance & Huether, 2014). Pharmaceutical therapy ultimately involves the prescription of monoamine oxidase B inhibitors, “dopamine agonists that directly stimulate dopamine receptors, anticholinergic drugs, antihistamines, and amantadines” that may reduce negative motor manifestations and improve the health condition of the patients with Parkinson’s disease (McCance & Huether, 2014). Catechol-O-methyltransferase (COMT) inhibitor aims to prolong the half-life of dopamine. In case of inefficient pharmacotherapy, practitioners can resort to such surgical interventions as thalamotomy and pallidotomy that can reduce troublesome motor symptoms at the latest stages of Parkinson’s disease. Deep brain stimulation can be beneficial when coping with medically resistant clinical manifestations and dyskinesia that result from levodopa intake. Presently, researchers continue developing gene- and cell-based therapies that can become critically promising treatment options for future medical management of Parkinson’s disease. Physical and speech therapies are also crucial in treating Parkinson’s disease patients, particularly at the advanced stages. Generally speaking, any kind of preventive, supportive, and symptomatic care assists in alleviating the symptoms characteristic of the given disorder and enhancing the functionality of the affected people.
In conclusion, Parkinson’s disease is a severe, incurable, multifactorial, and multi-system degenerative disorder that significantly disrupts the physiological and cognitive functions of the patient. It occurs due to the low or insufficient level of dopamine that is required for controlling motor functions. Resting tremors, postural instability, rigidity, impaired speech, and other autosomal, neuroendocrine, and cognitive symptoms characterize the clinical picture of Parkinson’s disease. Neurologists actively apply all available treatment options, including medication, surgical interventions, and deep brain stimulation for reducing severe motor symptoms of the disorder. Physiotherapy, speech therapy, and other innovative treatment methods can facilitate the rehabilitation of Parkinson’s disease patients and their overall health improvement.
Amyotrophic Lateral Sclerosis
Amyotrophic lateral sclerosis (ALS) is also a serious, progressive neurodegenerative disorder that can drastically worsen the health condition and reduce the life expectancy of aging people. It can primarily appear under the influence of many unfavorable factors that initiate the pathology. Thus, sufficient medical background regarding ALS can be beneficial for preventive care and educative purposes.
This disorder stems from the severely affected “motor areas of the cerebral cortex, axons of the upper motor neurons in the corticospinal and rubrospinal tracts,” and simultaneously attacked “lower motor neuron cell bodies” (Tortora & Derrickson, 2014). It is associated with considerable damage to the neuron networks that start disintegrating consistently and ultimately results in the systematic dismantling of the entire motor neuron system of the body.
Despite the unclear pathogenesis, multiple research allowed to specify oxidative stress, excessive glutamate release, neurofilament defects, mitochondrial malfunction, apoptosis, free radicals, neuroinflammation, deficient nerve growth factor, and autoimmune responses as the primary pathways that contribute to the pathophysiology of the disease in question. Moreover, some researchers indicate that glial cell pathology and aggregated abnormal proteins also entail ALS-associated motor neuron injuries (Armon, 2017). Viral infections, head traumas, and exposure to environmental toxins can also facilitate the progression of the disease under review. Additionally, various mutations in certain genes can trigger this disorder. Therefore, all indicated factors have detrimental effects on motor neuron functioning that induce the onset and further development of ALS.
Clinical manifestations of ALS slightly vary depending on which motor neurons are affected. In the case of lower motor neuron damage, the given disease manifests itself in gradual muscular atrophy that can result in paralysis. In this case, hypotonia, “hypoactive or absent deep tendon reflexes, and decreased or absent abdominal and cremasteric reflexes” are the prominent hallmarks of the studied affliction (McCance & Huether, 2014). Furthermore, such symptoms as fasciculations and fibrillations are frequently present in the affected people. Upper motor neuron injury appears in muscle spasticity that eventually becomes severe and entails muscular atrophy. It also manifests itself in “hyperactive deep tendon reflexes and clonus with extreme spasticity” as well as the present Babinski sign (McCance & Huether, 2014). Other symptoms are practically similar. Additionally, ALS patients suffer from impaired coordination, speech disturbances, difficulty swallowing and breathing, and decreased perspiration.
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Health care providers frequently prescribe antiglutamate medication for reducing symptoms and improving motor neuron functioning. Presently, they tend to administer Riluzole and Edaravone which can be efficient in reducing ASL symptoms and improving daily functioning. Competent treatment of ALS can provide relief, prevent complications, and enhance the health condition, although it cannot cure the disease. It ultimately assists in “maintaining optimal life quality” (Tortora & Derrickson, 2014). Supportive, preventive, and symptomatic care is crucial for medical management that can considerably prolong the life span of the people affected by ALS. Palliative care helps alleviate such symptoms as dysphagia, dysarthria, fasciculations, and depression that develop at later stages of the disorder.
In conclusion, amyotrophic lateral sclerosis is a severe degenerative disease that ensues from various impairments in the lower and upper motor neurons. The alterations related to ALS stem from genetic mutations and changes on the cellular level in the brain and spinal cord. The disease occurs due to excessive release of the neurotransmitter glutamate, oxidative stress, mitochondrial malfunction, and other multiple factors that contribute to ALS pathogenesis. Such markers as muscular spasticity, hypotonia, fasciculations, hyperactive or absent reflexes of the tendons, and absent abdominal, as well as cremasteric reflexes, help detect ALS. A range of efficient drugs, surgical interventions, and preventive, supportive, and symptomatic care is actively involved in relieving ALS-related symptoms and signs. All therapeutical interventions can prolong the patient’s life. However, scientists have to continue their research by developing medication and techniques that can be effective in curing the disease under discussion.