Otto Farquharson
BIO 3526 (Pathophysiology)
Project: Parkinson’s Disease
Background and Pathophysiology
Parkinson’s disease, also known as idiopathic parkinsonism, is a progressive neurodegenerative disease caused by a loss of dopamine neurons in the substantia nigra. Parkinsonism is the term used to refer to the clinical condition that occurs from the degeneration in the basal ganglia function. The word parkinsonism comes from the British physician James Parkinson. In 1817, Dr. Parkinson published a research paper in which he was the first to describe the disease. These dopamine neurons are responsible for creating dopamine, which is responsible for movement and motivation. The substantia nigra is located in the midbrain beneath the basal ganglia. These neurons normally communicate with the striatum in the brain. Along with the loss of these dopamine neurons, Lewy Bodies (clumps of protein) begin to form in these dopamine neurons. It is not yet known what role these clumps of proteins play in the disease. When the dopamine neurons are lost, there is less dopamine, which means less movement (see image on page 11). Movement can no longer be initiated as well, therefore movement is now altered. When 80% of these dopamine neurons are lost, this is when clinical manifestations begin to show. Examples of clinical manifestations include bradykinesia (slower movement), tremor, rigidity, jerky movement, and stooped posture. People with Parkinson’s disease also have issues with balance. These dopamine signals from the substantia nigra is responsible for amplification of the thalamus, which causes excitement of the person’s muscles, and makes them increase their movement (eg, faster and more forceful). Regardless of the clinical manifestations, Parkinson’s Disease can only be seen after the person has died, and an autopsy is completed.
Most people with Parkinson’s have no family history or genetic predisposition. However, research shows that a genetic loci known as PARK 1-9 and mutations of the genes (HTRA2, LRRK2, NR4A2, NDUFV2, ADH3, FGF20, GBA and MAPT) are associated with Parkinson’s disease (Thomas, 2007). However, less than 20 percent of people with the disease are carriers of a predisposing gene, which means that carrying the gene increases the risk, but most of the other factors are still unknown.
Parkinson’s disease can also be seen in narcotic addicts who’ve used 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP). It can also occur as a post-encephalitic syndrome from therapy with antipsychotic drugs that block dopamine receptors.
There is currently ongoing research about Parkinson’s Disease related to head trauma (See Data section).
Possible treatment pathways
Although there is no cure for Parkinson’s Disease, there are several ways to control it and prevent its progression. One way is through pharmological treatments such as Levodopa. Levodopa is a dopaminergic which assists to restore normal transmission of nerve impulses. This will improve akinesia and bradykinesia, allowing more smooth movements and better initiation of movements. Levodopa converts to dopamine in the basal ganglia, which will increase the overall dopamine level concentration in the brain. This medication is taken orally with meals to decrease gastrointestinal distress, which is one of the non-motor symptoms of Parkinson’s disease due to lack of movement. Some side effects of this medication can include anorexia, nausea, vomiting, behavioral disturbances, and postural hypotension. However, since many of those side effects will exacerbate the consequences of being bedridden (which happens in late Parkinson’s), the patient is advised to keep a diary to track scheduled dosages and effects. Therapeutic effects of Levodopa may take several weeks to months to show. This medication should never be discontinued abruptly.
Another medication that can be used, is Sinement. Sinement is levodopa with carbidopa, which is also a dopaminergic. It crosses the blood-brain barrier and converts to dopamine. Carbidopa inhibits the enzyme that would break down levodopa. Sinement can have adverse effects on the gastrointestinal system, including weight loss, nausea, and vomiting. Adverse effects of abnormal movements may occur if the patient overdoses. These movements occur from an overload of dopamine in the brain, and include bruxism (forceful clenching and grinding of the teeth), chorieform movements (involuntary jerky movements) and protruding of the tongue. Sinemet has a rapid onset and a duration of 6-12 hours. Patients must be educated to avoid foods high in vitamin B6 since they block the effects of anti-parkinsonian drugs.
Parkinson’s disease can also be treated with anticholingerics such as Cogentin. Cogentin inhibits parasymphatetic nerve impulses by blocking the action of acetylcholine at sites throughout the body and the central nervous system. The therapeutic effect is smoother movement for patients with Parkinson’s disease.
Deep brain stimulation is a relatively modern approach to people with Parkinson’s disease who respond to pharmacologic treatment but experience side effects such as unstable dyskinetic movements. In deep brain stimulation, electrodes are implanted into the pars interna of the globus pallidus or into the subthalamic nuclei. The purpose of deep brain stimulation is to stimulate the substhalamic nuclei for periods of time to allow for a smaller medication dose, hence improving the kinetic function of the person while decreasing the side effects of the drugs that they are taking to manage their Parkinson’s disease.
Research indicates that exercising regularly can be beneficial to people with Parkinson’s disease. Exercise reduces stiffness, improves mobility, balance, posture, gait, and reduces depression. (UCSF 2012). Brain exercises such as games that jog memory can help prevent cognitive deterioration.
Data:
According to the CDC, Parkinson’s Disease is the second most common neurodegenerative disease. In developed countries, the occurrence of Parkinson’s Disease is about 0.3 % of the population. The onset of Parkinson’s disease usually occurs after age 50. The frequency of the disease increases to about 4% or 5% in people above 85 years old. According to the Parkinson’s Disease Foundation, there are more than 10 million people living with Parkinson’s Disease worldwide, about 60,000 Americans are diagnosed each year, and about 4% are diagnosed before the age of 50. Men are also “one and a half times more likely to have Parkinson’s than women (Parkinson’s Disease Foundation 2016).” Approximately 1 in 6 people with Parkinson’s have a relative with the disease. Symptoms of Parkinson’s Disease may progress over a very long period, for example 25 years or more.
There is a correlation of traumatic brain injury with the development of Parkinson’s Disease. According to a recent study published in JAMA Neurology, people with previous head injuries were 3.5 more likely to develop Parkinson’s Disease than those who had no head injury. The study also showed that the longer a person was unconscious, the faster the progression of Parkinson’s (up to 2 times faster) than those who had no head trauma. “Even a single head injury with loss of consciousness puts people at pretty remarkably increased risk of Parkinson’s disease (Crane 2016).”
The National Parkinson Foundation is currently conducting a study called the Parkinson’s Outcomes Project. This research is aimed at improving the lives of people diagnosed with Parkinson’s Disease. This study involves almost 10,000 patients in 4 countries. According to the results of this study, exercise provides neuroprotective benefits that could alter the path of the disease. The patient should have at least 2.5 hours of physical activity per week. The two biggest issues which increased the rate of declination of the patients’ bodies, were anxiety and depression.
According to the CDC, continuing studies are showing that Parkinson’s Disease is less common in coffee drinkers and cigarette smokers.
Discussion:
According to the National Parkinson’s Foundation, there are five stages of Parkinson’s Disease. The first stage is very mild, and the person can perform their daily activities normally. However, there is noticeable unilateral tremor, a slight alteration in posture, and slight facial grimacing. In the second stage of Parkinson’s, the tremor becomes bilateral and more time is needed to complete everyday tasks. “The tremor may manifest as a rhythmic, slow turning motion (pronation–supination) of the forearm and the hand and a motion of the thumb against the fingers as if rolling a pill between the fingers (Smeltzer 2010).” Although ordinary tasks are more difficult to complete, the person can still remain independent. In the third stage, the person has a significant reduction in speed and balance. Simple tasks such buttoning a shirt and eating with a fork or spoon become increasingly difficult and or even frustrating. At this stage, the person is also at risk for falls due to their shuffling gait. In the fourth stage, the person is no longer independent. They may require assistive walking devices due to severe imbalance. They can no longer perform most activities of daily living on their own. The fifth stage is the most critical stage. The person may be confined to bed, unable to stand or walk (due to resistance to passive limb movements) and they now require 24-hour care for every activity. In stage five, the person will have drooling, difficulty chewing and swallowing, poor gag reflex, increased oral secretions, difficulty initiating movement (ataxia), slurred/mumbled speech, hallucinations, memory lapses, delusions, depression, irritability, sleep disorders, and possibly dementia.
Due to ataxia, slower swallowing and excess saliva production, a person with late stage Parkinson’s Disease is at risk for aspiration. Aspiration is a condition in which food, liquids, or saliva is breathed into the larynx, which can be fatal. To avoid this, patients with Parkinson’s Disease are given medication priority. This is to make sure that their medications are given on time so that they get the next dose before the previous one completely wears off.
Future research/Future direction
Future research on Parkinson’s disease is geared mostly toward preventative care and secondary treatments. These include gene therapy, neuroprotective therapies, identification of Biomarkers, and neural transplantation (Holland, 2016).
According to Healthline, a new device called the Brio Neurostimulation System was recently approved by the Food and Drug Administration. This is a tiny implantable device that is able to generate minute electrical pulses throughout the body to help reduce the symptoms of Parkinson’s disease. This system however, is not yet widely available. Neural transplantation, another new direction of Parkinson’s Disease research, is the method in which dying brain cells are replaced with new cells that can grow and proliferate. However, this type of treatment is still a very long way off since trials showed that some patients improved significantly, while other patients became worse. Clinical trials are still ongoing.
Why I chose this topic
When I was a young child, anytime I spent time with my grandfather I would notice that he was always “shaky” when doing things, especially with his hands. Whether it was handing me something, putting on his hat, using the remote control, or opening the door with keys, he always had this mysterious uncontrollable shaking. I used to think it was just a normal part of his life, but looking back now, he was probably in the second stage of the disease. Then one day at the age of 8, I climbed a fence in my elementary school playground, fell off and landed on my hand flexed outward. This resulted in a wrist-sprain injury. With this injury, I had a slight tremor in same hand for a few months afterward and became scared because I thought that I would end up just like my grandfather very soon. It made me ask my mother a lot of questions about my grandfather’s “shaky” condition. Even though my mild hand tremor went away after a few months, from then onward, I always had an interest in the origins of Parkinson’s Disease.
Fast forward 20 years later, I’m now a Registered Nurse in orientation at a long term care and rehabilitation center. While in nursing school, I had the privilege of creating several care plans for patients with neurological disorders including Parkinson’s Disease (see pages 9 and 10). I expect to use this care plan on future patients as well. Every day I am seeing more and more of why it is important for an aging person to make every effort to stay as physically and mentally active as possible.
Care Plan for the patient with Parkinson’s Disease
Assessment | Diagnosis | Outcome criteria | Intervention | Evaluation |
-Patient has a shuffling gait
-Difficulty initiating movement, and slowness of voluntary movements
|
-Risk for falls
-Impaired physical mobility
-Impaired walking
-Risk for injury related to unstable body movement |
-Patient will demonstrate maximum independent physical mobility and ADL function. | -Assist patient with using footwear that prevents falls/injury
-Teach patient to maintain a wide stance while walking to avoid shuffling and falling.
-Create clear, uncluttered walking paths
-Teach patient to swing arms while walking
-Teach patient to rock back and forth to initiate movement
|
-Patient maintains independence in walking (with or without assistive devices) and carrying out ADLs. |
-Patient has increased secretions | -Risk for aspiration related to pooled secretions
-Impaired swallowing
|
-Patient will effectively handle oral secretions and remain free of aspiration. | -Have suction equipment nearby to remove secretions to prevent choking.
-Provide oral hygiene |
-Patient maintains good oral hygiene, remains free of aspiration and respiratory infections such as pneumonia |
-Patient has difficulty chewing and swallowing, has poor gag reflex, and is losing weight.
|
-Imbalanced nutrition: less than body requirements related to dysphasia | -Patient will maintain adequate nutritional intake. | -Assess ability to swallow
-Collaborate with speech and occupational therapist.
-Ascertain positive gag reflex before feeding patient.
-Offer small portions of easily chewed foods, high in calories and protein. (semisolid diet with thick liquids)
-Maintain patient in sitting position for feedings. -Allow ample time for eating |
-Patient swallows without aspiration, takes time while eating, and maintains body weight in normal parameters. |
-Patient has rigidity
-Patient has tremor at rest in extremities and head. |
-Impaired physical mobility
-Risk for injury related to rigidity, tremors and jerky movements |
-Patient will remain free of injury | -Perform stretch-hold exercises to help reduce or prevent contractures.
-Assess handwriting ability
-Avoid rushing patient during activities
|
-Patient participates in daily exercise program, remains free from injuries, and adheres to medication regimen |
-Patient is unable to speak clearly (slurred, mumbled and low volume), has a lack of facial expression, and gets frustrated when asked to repeat things. | -Impaired verbal communication related to Parkinson’s disease. | -Patient will be able to effectively communicate needs and converse with family and staff. | -Keep background noise to a minimum while patient is speaking
-Collaborate with speech therapist. Allow ample time for patient to speak.
-Do not finish sentences for the patient (will cause frustration)
-Avoid shouting while talking to patient. -Use simple phrases
|
-Family and staff are able to understand patient’s verbal phrases. Patient practices speech exercises |
-Patient shows late mental deterioration
|
-Ineffective coping
-Risk for caregiver role strain
-Acute confusion
-Risk for injury |
-Patient will remain free of injury
-Family or caregiver will effectively cope with patient’s deteriorating condition |
-Assess neurological status
-Keep patient well hydrated
-Assess vital signs and temperature to rule out infection (fever)
-Keep environment free of hazards to minimize risk for injury due to confusion
-Assess changes in medication dosages
-Avoid activities that increase frustration
-Reassure family or caregiver that Parkinson’s is a neurodegenerative disease, which may come with late mental deteriorations
|
-Patient is oriented and exhibits no evidences of hallucinations or delusions. Family remains calm if hallucination occurs. |
References
Crane PK, Gibbons LE, O’Connor KD et al. 2016. Association of traumatic brain injury with
late-life neurodegenerative conditions and neuropathologic findings. JAMA Neurol
73(9):1062-1069.
Centers for Disease Control and Prevention. (2011). Genetics, coffee consumption, and
Parkinson’s disease. Retrieved November 21, 2016 from
https://www.cdc.gov/genomics/hugenet/casestudy/parkinson/parkcoffee_view.htm
Healthline. (2016). Advanced and Future Treatments for Parkinson’s. Retrieved November 28,
2016 from http://www.healthline.com/health/parkinsons/future-treatments#2
Lewis SM, Dirksen SR. 2011. Medical-Surgical Nursing: Assessment and management of
clinical problems. 8th ed. St. Louis (MO): Elsevier/Mosby.
National Parkinson Foundation. (2016). The Stages of Parkinson’s Disease. Retrieved November
28, 2016 from http://www.parkinson.org/understanding-parkinsons/what-is-
parkinsons/The-Stages-of-Parkinsons-Disease
Osborn KS, Wraa CE. 2010. Medical-surgical nursing: Preparation for practice. 2nd ed. Boston
(MA): Pearson.
Parkinson’s Disease Clinic and Research Center: University of California, San Francisco. (2012).
Exercise and Physical Therapy for Parkinson’s Disease. Retrieved November 25, 2016, from
http://pdcenter.neurology.ucsf.edu/sites/pdcenter.neurology.ucsf.edu/files/excercise_and_ph
ysical_therapy_2012_web.pdf
Parkinson’s Disease Foundation. (2016). Statistics on Parkinson’s. Retrieved November 14, 2016
from http://www.pdf.org/en/parkinson_statistics
Porth CM, Matfin G. 2009. Pathophysiology: Concepts of Altered Health States. 8th ed.
Philadelphia (PA): Lippincott Williams & Wilkins.
Smeltzer SC, Bare BG. 2010. Brunner & Suddarth’s Textbook of Medical-Surgical Nursing. 12th
- Philadelphia (PA): Lippincott Williams & Wilkins.
Thomas B, Beal MF. 2007. Parkinson’s disease. Human molecular genetics, Vol. 16, Review
Issue 2: R183-R194.