You Work For A Neuropsychologist With Patients Who Have Been

You Work For A Neuropsychologist With Patients Who Have Been Diagnosed

You work for a neuropsychologist with patients who have been diagnosed with Parkinson’s disease or Huntington’s disease. You have been asked to educate the patients and their family members about the diseases. Select either Parkinson's disease or Huntington’s disease as your topic, and research information about the disease. Describe the disease. Describe the roles and functions of the human nervous and endocrine systems in relation to the disease. Explain why the disease interrupts an individual’s ability. Describe the behaviors that are typically exhibited following the onset of the disease. Describe the deficits typically seen because of the disease. Describe treatment options available for individuals with the disease. Explain the current research findings related to outcomes of the disease.

Paper For Above instruction

Parkinson’s disease is a progressive neurodegenerative disorder primarily characterized by the loss of dopamine-producing neurons in the substantia nigra, a part of the midbrain. This disease affects movement control, leading to symptoms such as tremors, rigidity, bradykinesia, and postural instability. Parkinson’s disease generally manifests in individuals over the age of 60, though early-onset cases may occur, involving complex interactions between genetic and environmental factors (Kalia & Lang, 2015). The pathology of the disease centers on the degeneration of dopaminergic pathways, which disrupts the basal ganglia circuits responsible for initiating and controlling voluntary movements (Jankovic, 2008).

The human nervous system plays a pivotal role in Parkinson’s disease. The central nervous system (CNS) facilitates motor control through interconnected pathways involving the basal ganglia, cerebral cortex, and substantia nigra. A deficiency of dopamine inhibits these circuits, impairing motor functions. The autonomic nervous system, a component of the peripheral nervous system, also influences non-motor symptoms such as blood pressure regulation, gastrointestinal function, and sleep, all of which can be affected in Parkinson’s patients. The endocrine system interacts indirectly with the nervous system; for instance, abnormal dopamine levels can influence hormonal pathways, contributing to symptoms like depression or sleep disturbances (Chaudhuri & Schapira, 2009).

Parkinson’s disease significantly interrupts an individual’s ability to perform daily activities. Motor deficits result in difficulties with walking, balance, and fine motor tasks like writing or buttoning clothes. These impairments increase the risk of falls and injuries, contributing to loss of independence. Non-motor symptoms such as cognitive impairment, mood disorders, sleep disturbances, and autonomic dysfunction further compromise quality of life. As the disease progresses, individuals often experience difficulties with speech, swallowing, and maintaining their personal and social activities (Hely et al., 2013). These symptoms collectively hinder an individual’s ability to work, engage socially, and perform routine self-care.

Behavioral changes following the onset of Parkinson’s disease are notable. Patients may exhibit depression, anxiety, apathy, or cognitive decline, especially in advanced stages. Psychosis, hallucinations, and impulse control disorders can also develop as side effects of medication treatments, particularly dopamine agonists. Motor symptoms such as tremors and rigidity are often accompanied by fatigue and reduced initiative, which can strain familial and social relationships (Leroi et al., 2012). These behavioral changes call for comprehensive management involving pharmacological and psychosocial interventions.

The deficits caused by Parkinson’s disease include bradykinesia, rigidity, resting tremors, and postural instability. Cognitive deficits may involve executive dysfunction, slowed processing, and memory issues. Non-motor deficits encompass autonomic dysfunction (e.g., orthostatic hypotension), sleep disturbances, and behavioral changes (Beecham et al., 2014). These deficits result from neurodegeneration within specific brain regions, primarily the substantia nigra, but also involve other areas such as the locus coeruleus and the cholinergic system, which contribute to cognitive and autonomous functions (Schapira et al., 2014).

Treatment options for Parkinson’s disease aim to manage symptoms and improve quality of life. Pharmacologically, levodopa remains the most effective treatment, often combined with carbidopa to enhance central nervous system availability. Dopamine agonists, MAO-B inhibitors, and COMT inhibitors extend the beneficial effects of levodopa and help control motor fluctuations. Deep brain stimulation (DBS), a surgical intervention, involves implanting electrodes in specific brain regions to regulate abnormal activity. Additionally, physical therapy, occupational therapy, and speech-language therapy are crucial in maintaining mobility, communication, and functional independence (Weintraub et al., 2018). Non-pharmacological approaches, such as exercise and dietary adjustments, also support symptom management and overall well-being.

Current research on Parkinson’s disease focuses on understanding its pathogenesis, early detection, and developing disease-modifying therapies. Recent advances include the identification of genetic risk factors, such as mutations in the LRRK2 and SNCA genes, which contribute to familial forms of the disease (Kumar et al., 2018). Biomarker research aims to facilitate earlier diagnosis and monitor disease progression more accurately. Moreover, novel therapeutic approaches such as gene therapy, stem cell transplantation, and neuroprotective agents are under investigation. Clinical trials are examining drugs that target alpha-synuclein aggregation, a hallmark of Parkinson’s pathology, with promising results toward halting or slowing disease progression (Olanow et al., 2020). Ultimately, the goal of current research is to transition from symptomatic treatment to disease-modifying strategies that can alter the course of Parkinson’s disease.

In summary, Parkinson’s disease is a complex neurodegenerative disorder that profoundly impacts motor, cognitive, and autonomic functions through its effects on the nervous and endocrine systems. Effective management involves a combination of medication, surgical interventions, and supportive therapies, with ongoing research promising new avenues for treatment and potential cures. Awareness and education about these aspects are crucial for patients and their families to navigate the challenges posed by the disease and to optimize quality of life.

References

• Beecham, G. W., Kaur, T., & Loke, Y. J. (2014). The genetics of Parkinson's disease: progress and prospects. Human Molecular Genetics, 23(R1), R51-R58.
• Chaudhuri, K. R., & Schapira, A. H. V. (2009). Non-motor symptoms of Parkinson’s disease: dopaminergic pathophysiology and treatment. The Lancet Neurology, 8(5), 464-474.
• Hely, M. A., Shepherd, T., & Chapman, J. (2013). The Sydney multicenter study of Parkinson’s disease: The inevitability of disability and the importance of support. Movement Disorders, 28(5), 585-592.
• Jankovic, J. (2008). Parkinson’s disease: clinical features and diagnosis. Journal of Neurology, Neurosurgery & Psychiatry, 79(4), 368-376.
• Kalia, L. V., & Lang, A. E. (2015). Parkinson’s disease. The Lancet, 386(9996), 896-912.
• Kumar, N., et al. (2018). The emerging genetics of Parkinson disease. Nature Reviews Neurology, 14(5), 283-297.
• Leroi, A. M., et al. (2012). Behavioral and psychological symptoms in Parkinson’s disease. Journal of Parkinson’s Disease, 2(4), 403-411.
• Olanow, C. W., et al. (2020). Gene therapy in Parkinson’s disease: the future of disease modification. Movement Disorders, 35(4), 531-543.
• Schapira, A. H. V., et al. (2014). Neurobiology of Parkinson’s disease. Nature Reviews Neuroscience, 15(4), 262-278.
• Weintraub, D., et al. (2018). Treatment of motor and non-motor symptoms of Parkinson’s disease. UpToDate.