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Parkinson’s Disease and Huntington’s Disease
There are many neurological diseases, many of which can have both similarities and of course differences. Two neurological diseases that can be compared are Parkinson’s disease and Huntington’s disease. Both can be seen as neurodegenerative, which progresses over time. One of the main features of Parkinson’s is loss of dopaminergic neurons and activity, as well as an increase in cholinergic activity. Likewise, dopaminergic neurons are also affected in Huntington’s, leading to uncontrolled movements (Tampia et al., 2021). De la Cruz and Hwang (2021) discuss the genetic aspect of Huntington’s disease, stating how it is an inherited autosomal dominant disease, affecting chromosome four. Therefore, there is an increased risk with a family history of the disease. McCance and Huether (2019) discusses how there are many different genetic mutations that can happen to lead to Parkinson’s. To add, Parkinson’s disease shows symptoms of “tremor, stiffness, slowness, balance problems and/or gait disorders” as well as mental issues like loss of memory and hallucinations and issues with the bladder (Duncan, 2021 p. 251). There are both neuropsychiatric symptoms and motor symptoms that can arise with Huntington’s. Some of the first symptoms are neurological, such as decline in mental status, depression and irritability (Tampi et al., 2021) Chorea can be one of the first motor symptoms in Huntington’s (Tampi et al., 2021).. One can see chorea as uncontrollable movements that almost look like a dance like movement and can be seen in both diseases. Both diseases lead to a decrease in life expectancy once diagnosed. Those with Huntington’s usually do not know until after the age of 40 and overtime and those with Huntington’s usually are diagnosed between 25 and 40 and develop progressive dementia (McCance & Heuther, 2019). There are no known cures for both diseases. Therefore, the main focus is management of symptoms. For example Duncan (2021) discusses how utilizing drugs such as levodopa, which work to increase dopamine, and how the bladder issues and training on exercises can be done to help with Parkinson’s. Dopamine affects motor symptoms and movement, and therefore the use of levedopa helps towards improving motor symptoms (Greig & McKeage, 2016). Similarly, Huntington’s disease symptoms are managed. For example, treating one of the hallmark symptoms of chorea can be the focus with medication. Both diseases not only affect the patient, but the family as well. There is currently no cure for Parkinson’s disease (Duncan, 2021). Likewise, there is no cure for Huntington’s disease (Tampi et al., 2021). As stated earlier, issues with one’s bladder can become a problem for patients with Parkinson’s disease, as well as many other symptoms.
It is clear that there are many issues and symptoms that arise in patients who have these diseases. The diseases usually progress, causing hardship on the patient and the families. Educating families on the disease, the symptoms, and managing the symptoms can be key. Providing emotional support and encouraging self-care for the caregiver are also important interventions for families caring for their loved one.
De la Cruz, J., & Hwang, J. (2021). On the hunt for a cure. Journal of the American Academy of Physician Assistants, 34(4), 26-31.
Duncan, D. (2021). Role of the community nurse in Parkinson’s disease and lower urinary disorders. British Journal of Community Nursing, 26(5), 251-254.
Greig, S. L., & McKeage, K. (2015). Carbidopa/Levodopa ER capsules (Rytary®, Numient™): A review in Parkinson’s disease. CNS Drugs, 30(1), 79-90.
McCance, K. L., & Huether, S.E. (2019). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). Mosby Elsevier.
Tampi, R. R., Weber, M., & Masterson, G. A. (2021). Early warnings: Neuropsychiatric manifestations of Huntington disease. Psychiatric Times, 38(3), 25-27.
The neurodegenerative disorders of Parkinson’s disease (PD) and Huntington’s disease (HD) share some characteristics but are also different in many ways as the distinct structures within the basal ganglia of the brain, an area involved in movement regulation, are differently affected. In both PD and HD, the deregulation of the movement circuitry due to loss of the specific neuronal populations in basal ganglia is the underlying cause of motor symptoms due to the loss of of dopaminergic neurons of the substantia nigra par compacta and the GABAergic neurons of the striatum in PD and HD, respectively (Troncoso-Escudero et al., 2020). These diseases share some factors, but the ability to distinguish them and provide proper treatment is important.
HD is an an autosomal dominant disorder that is caused by the elongation of CAG repeats on the short arm of a chromosome in the HTT gene which encodes for the protein (Jimenez-Sanchez et al., 2017). Additionally, the primary feature is the degeneration of neurons in the putamen, caudate, and cerebral cortex which leads to chorea, dystonia, and akinesia (Jimenez-Sanchez et al., 2017). HD generally affects patients between the ages of 30 to 50 and consists of motor, cognitive, and psychiatric disturbances. The motor symptoms are progressive and include hyperkinetic with involuntary movements of chorea, beginning distally of small degree and then become more axial and are of greater amplitude (Jimenez-Sanchez et al., 2017). Psychiatric symptoms associated with HD are consistent with frontal lobe dysfunction and include poor attention, irritability, impulsivity, poor mood regulation, and depression (Jimenez-Sanchez et al., 2017). Although there is no treatment, symptom management of HD includes medications to keep symptoms under control such as the drug Tetrabenazine, antipsychotic drugs, and antidepressants alongside rehabilitation strategies such as speech, occupational, and cognitive therapy (Bachoud-Lévi et al., 2019).
PD is also an an autosomal dominant disorder that is pathologically characterized by loss of nigrostriatal dopaminergic innervation, but that has a later onset and slower disease progression (Emamzadeh & Surguchov, 2018). Currently diagnosis is based on clinical symptoms with the criteria for diagnosis requiring the presence of two of the following clinical features: resting tremor, bradykinesia, rigidity and/or postural instability with a definitive diagnosis being made by histopathological assessment with the identification of α-synuclein-containing Lewy bodies (Emamzadeh & Surguchov, 2018). Although no cure exists, similarly to HD, treatment of PD is based on symptoms and needs and consists of medication that enhances dopamine levels, such as Levodopa or Carbidopa/Levodopa, surgery consisting of deep brain stimulation therapy, and gene therapy (Emamzadeh & Surguchov, 2018). Speech, occupational, and cognitive therapies may also be beneficial for these individuals.
As providers, we can assist families in their journey of caring for family members with these diseases by exploring concerns, providing an empathetic approach, and most importantly educating the diagnosed individual and his or her caregivers about disease progression and what to expect. It is important to prompt family to share their concerns and questions in relation to the disease so that there is no confusion. Additionally, providers can build a foundation of trust with the family and patient, and be available to answer further questions when they present themselves.
Bachoud-Lévi, A. C., Ferreira, J., Massart, R., Youssov, K., Rosser, A., Busse, M., Craufurd, D., Reilmann, R., De Michele, G., Rae, D., Squitieri, F., Seppi, K., Perrine, C., Scherer-Gagou, C., Audrey, O., Verny, C., & Burgunder, J. M. (2019). International guidelines for the treatment of Huntington’s disease. Frontiers in Neurology, 10, 710. https://doi.org/10.3389/fneur.2019.00710 (Links to an external site.)
Emamzadeh, F. N., & Surguchov, A. (2018). Parkinson’s disease: Biomarkers, treatment, and risk factors. Frontiers in Neuroscience, 12, 612. https://doi.org/10.3389/fnins.2018.00612 (Links to an external site.)
Jimenez-Sanchez, M., Licitra, F., Underwood, B. R., & Rubinsztein, D. C. (2017). Huntington’s disease: Mechanisms of pathogenesis and therapeutic strategies. Cold Spring Harbor Perspectives in Medicine, 7(7), a024240. https://doi.org/10.1101/cshperspect.a024240 (Links to an external site.)
Troncoso-Escudero, P., Sepulveda, D., Pérez-Arancibia, R., Parra, A. V., Arcos, J., Grunenwald, F., & Vidal, R. L. (2020). On the right track to treat movement disorders: Promising therapeutic approaches for Parkinson’s and Huntington’s disease. Frontiers in Aging Neuroscience, 12, 571185. https://doi.org/10.3389/fnagi.2020.571185
Parkinson’s disease (PD) is a progressive neurodegenerative disorder. It is known to begin around 40 years of age or later and increases after 60 years (McCance & Huether, 2019). There are two forms, familial, which can be inherited in autosomal dominant or recessive manner, and sporadic, also known as idiopathic, which is believed to develop based on gene-environment interactions (Ball et al., 2019). Sporadic Parkinson’s Disease makes up majority of cases. The etiology of Parkinson’s disease is unknown, although there have been several gene mutations that have been identified (McCance & Huether, 2019). PD is due to a loss of nerve cells in the brain known as substantia nigra (Jagadeesan et al., 2017). The nerve cells that are lost result in a lack of dopamine, which leads to motor complications and beginning of a slow progress, that gradually increases over years. As McCance and Huether (2019) describe, the primary pathology is degeneration of the basal ganglia with the formation of Lewy bodies, which then leads to the loss of dopamine filled neurons, as mentioned earlier. Classic symptoms of PD include, resting tremor, muscle rigidity, loss or movement and postural instability (Ball et al., 2019). Non-motor symptoms can include depression, hypotension, loss of sense of smell, anxiety, or panic attacks (Jagadeesan et al., 2017). The non-motor symptoms can present before the motor symptoms do and can be key in identifying and diagnosing PD early (Ball et al., 2019). Treatment includes reducing and treating symptoms. This can include drug therapy to restore dopamine levels and manage both motor and nonmotor symptoms. For example, medications like levodopa that increase the level of dopamine in the brain can be used. Other drugs such as anticholinergic agents interfere with the production of acetylcholine which can help reduce tremors, which usually occur when one has more acetylcholine than dopamine in their system (Jagadeesan et al., 2017).
Huntington’s disease (HD) is also a neurodegenerative disease, where there is a dominantly inherited cytosine-adenine-guanine (CAG) trinucleotide repeat expansion in the huntingtin gene on chromosome 4 which results in a mutant huntingtin protein (Tabrizi et al., 2019). Like Parkinson’s disease it does involve the basal ganglia, and is characterized by movement disorder, behavioral symptoms and cognitive decline (Tabrizi et al., 2019). However, unlike Parkinson’s disease, the onset occurs earlier, around 25 to 45 years of age (McCance & Huether, 2019). HD occurs due to the production of the mutant huntingtin protein, with a long polyglutamine repeat (McColgan & Tabrizi, 2017). As McCance and Huether (2019) describe, “Expression of the huntingtin gene produces tangles of protein that collect in brain cells and chains of glutamine on the abnormal molecules that adhere to each other.” The mutant huntingtin gene results in neuronal dysfunction and death which leads to the progressive movement, behavior, and cognitive symptoms (McColgan & Tabrizi, 2017). HD can be diagnosed with confirmation of family history or a positive genetic test. Symptoms of HD can progress slowly and include involuntary movements, similarly to Parkinson’s disease. Chorea, the abnormal movement of the face and arms, is the most prominent symptom and occurs early in the disease (McColgan & Tabrizi, 2017). Cognitive decline can occur as well, such as loss of memory and the capacity to plan, restlessness, irritability, and depression (McCance & Huether, 2019). There are no treatment options on halting the progression of Huntington’s disease, but drug therapies are available to treat the symptoms.
Parkinson’s disease and Huntington’s disease do have similarities due to being neurogenerative diseases. For families, it can be a challenge caring for their family members when symptoms begin to worsen. It is important that the family members or caregivers feel supported in their journey with a family member with such diseases. First, they should be prepared by learning about the disease and what to expect. They should know that they should seek help, and not try to do everything on their own for their family member and should be told to remember their personal health too. They can best help their family member if they take care of themselves first. They should also be educated on attending support groups, as a way to voice their experiences and cope.
Ball, N., Teo, W.-P., Chandra, S., & Chapman, J. (2019). Parkinson’s disease and the environment. Frontiers in Neurology, 10(1). https://doi.org/10.3389/fneur.2019.00218
Jagadeesan, A. J., Murugesan, R., Vimala Devi, S., Meera, M., Madhumala, G., Vishwanathan Padmaja, M., Ramesh, A., Banerjee, A., Sushmitha, S., Khokhlov, A. N., Marotta, F., & Pathak, S. (2017). Current trends in etiology, prognosis and therapeutic aspects of Parkinson’s disease: A review. Acta Biomedical, 88(3), 249–262. https://doi.org/10.23750/abm.v88i3.6063
McCance, K. L., & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). Mosby Elsevier.
McColgan, P., & Tabrizi, S. J. (2017). Huntington’s disease: A clinical review. European Journal of Neurology, 25(1), 24–34. https://doi.org/10.1111/ene.13413
Tabrizi, S. J., Leavitt, B. R., Landwehrmeyer, G. B., Wild, E. J., Saft, C., Barker, R. A., Blair, N. F., Craufurd, D., Priller, J., Rickards, H., Rosser, A., Kordasiewicz, H. B., Czech, C., Swayze, E. E., Norris, D. A., Baumann, T., Gerlach, I., Schobel, S. A., Paz, E., & Lane, R. M. (2019). Targeting Huntingtin expression in patients with Huntington’s disease. New England Journal of Medicine, 380(24), 2307–2316. https://doi.org/10.1056/nejmoa1900907
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