Understanding Parkinson Disease: a complex and multifaceted illness.
Parkinson disease is an incredibly complex and multifaceted illness affecting millions of people in the United States. Parkinson disease is characterized by progressive dopaminergic neuronal dysfunction and loss, leading to debilitating motor, cognitive, and behavioral symptoms. Parkinson disease is an enigmatic illness that is still extensively researched today to search for a better understanding of the disease, develop therapeutic interventions to halt or slow progression of the disease, and optimize patient outcomes. This article aims to examine in detail the normal function of the basal ganglia and dopaminergic neurons in the central nervous system, the etiology and pathophysiology of Parkinson disease, related signs and symptoms, current treatment, and finally, the profound impact of understanding the disease on nursing care.
Keywords: dopamine neuron, levodopa treatment, movement disorders, MPTP Parkinson, Parkinson disease, Parkinson disease treatment, PD genes, substantia nigra
Parkinson disease (PD) is a progressive degenerative disorder of the central nervous system (CNS), in which motor functions are heavily debilitated. Motor symptoms, including tremor, rigidity, and bradykinesia, are the most common presenting symptoms. Other symptoms of PD typically develop later as the disease progresses and include cognitive, mood, and behavioral difficulties (Jankovic, 2008). There have not been any concrete causes established; however, evidence suggests that there are likely genetic and environmental factors contributing to the development and progression of PD. Less than 10% of PD cases are caused by known genetic mutations (Gandhi, Chen, & Wilson-Delfosse, 2009). Of the many environmental factors examined as causative agents of PD, insecticide and pesticide exposure are the only factors consistently implicated. Researches exploring gene-gene and gene-environment interactions in PD development and progression are ongoing.
PD is a very prevalent disease; there are about 7-10 million people in the world living with PD, of which more than one million live in the United States. Men are at a greater risk for developing PD than women (Parkinson's Disease Foundation, 2014). The disease incidence increases with age, with most symptoms developing after the age of 60 years; however, there has been an increase in presentation of PD symptoms with subsequent diagnosis before the age of 50 years. PD is the 14th leading cause of mortality in the United States (National Parkinson Foundation, 2014).
PD has a significant economical burden on the patients and families as well as the United States. It is estimated that the cost of PD in the United States is more than $25 billion annually, including medical expenses, lost income, and nursing home care (Parkinson's Disease Foundation, 2014). Flowever, the burden of the disease on the patient and family is immeasurable.
Although there is no cure for PD, medical management slows the progression of the irreversible disease while experts and researchers continue to search for groundbreaking restorative therapies. This article investigates the etiology and pathophysiology of PD at the cellular level and links the pathology to the various symptoms and current treatment options for the disease.
Normal Basal Ganglia Function
Research has confirmed that symptoms of PD are a result of progressive dopaminergic cell death in the substantia nigra pars compacta of the basal ganglia (Bergman & Deuschl, 2002). To fully comprehend the pathologic changes leading to symptoms of PD, a clear understanding of the normal function of the basal ganglia is important. The basal ganglia are a set of structures within the midbrain with connections that extend out toward the temporal lobe and up to the lateral ventricles (Herrero, Barcia, & Navarro, 2002). It consists of several structures, including the striatum (entailing the caudate and putamen), the globus pallidus (divided into internal and external segments), the substantia nigra, and the subthalamic nucleus (Herrero et al., 2002).
The striatum is the largest structure of the basal ganglia, receiving signals from various areas of the cerebral cortex and sending efferent signals to other structures of the basal ganglia. Impulses from various portions of the cerebral cortex, including the motor cortex, synapse on neurons of the striatum of the basal ganglia, releasing the excitatory neurotransmitter glutamate (Herrero et al., 2002). Glutamate stimulates the receiving neuron of the striatum to carry the impulse on to other areas of the basal ganglia. Specifically, the neurons of the striatum extend to the internal globus pallidus (direct pathway), the external globus pallidus (indirect pathway), and the substantia nigra (indirect pathway). Striatal neurons connecting to the globus pallidus and substantia nigra release gamma-aminobutyric acid (GABA), an inhibitory neurotransmitter. GABAergic inhibition of the pars reticularis substantia nigra neurons leads to further GABAergic inhibition of the thalamus, ultimately stimulating glutamatergic impulse transmission to the cerebral cortex (Herrero et al., 2002). In addition, GABAergic inhibition of the substantia nigra, and specifically, the pars compact region containing dopaminergic neurons, stimulates striatal input to both the external globus pallidus and the internal globus pallidus. Both segments of the globus pallidus receive input from the striatum and send output to the cortex through different pathways. Neurons of the internal globus pallidus utilize GABA to inhibit the thalamus, thereby communicating with the cerebral cortex (Herrero et al., 2002). The external globus pallidus extends GABAergic neurons to the subthalamic nuclei, a structure of the basal ganglia that utilizes the excitatory neurotransmitter glutamine to promote impulse transmission to the internal globus pallidus, which inhibits input to the thalamus and ultimately sends excitatory impulses back to the cortex (Bolam, Hanley, Booth, & Bevan, 2000). These structures of the basal ganglia receive and send signals to each other within the basal ganglia and to the cortex, producing coordinated, smooth, and fluid movements.
Dopamine is produced in the neurons of the pars compacta region of the substantia nigra within the basal ganglia, but also in other areas of the CNS and throughout the body (Herrero et al., 2002). Dopaminergic neurons in the limbic structures are heavily utilized in cerebral reward systems and dopamine modification of prefrontal working memory. The dopaminergic nigrostriatal pathway has been linked to the symptoms of PD (Bergman & Deuschl, 2002) because this pathway connects the substantia nigra (the source of dopaminergic neurons) with other parts of the basal ganglia and brain, facilitating coordinated movement. In the basal ganglia, there exist two pathways, one direct and the other indirect, with opposite effects on neuronal transmission.
In the direct pathway (Figure 1, available as Supplemental Digital Content 1 at http://links.lww.com/JNN/A38), the striatum, which receives excitatory stimulus from the cerebral cortex, projects increased inhibitory impulses to the internal segment of globus pallidus and substantia nigra, which in turn decrease impulses sent to the thalamus (Helie, Chakravarthy, & Moustafa, 2013). The normal function of the globus pallidus and substantia nigra is to inhibit the thalamus; when the two structures are disinhibited, the thalamus sends increased excitatory impulses to the cortex, propagating excitation of motor neurons. The net effect of this direct pathway is excitation and/or facilitation of movement (Rodriguez-Oroz et al., 2009).
In the indirect pathway (Figure 2, available as Supplemental Digital Content 2 at http://links.lww.com/JNN/A39), the striatum projects inhibitory neurons to the external globus pallidus, which projects inhibitory neurons to the subthalamic nucleus. The subthalamic nucleus projects excitatory neurons to the internal globus pallidus, which then sends inhibitory signals to the thalamus and, ultimately, the cortex (Helie et al., 2013). Loss of these striatal inhibitory effects results in decreased inhibition of the subthalamic nucleus and therefore increased internal globus pallidus stimulation, ultimately inhibiting thalamic stimulation of the motor cortex. The net effect of the indirect pathway is inhibition of some motor impulses, resulting in smoother, coordinated motor movement (Rodriguez-Oroz et al., 2009). Normally, there is a balance between the direct and indirect pathways.
It is important to note that the basal ganglia play additional roles in the body. Beyond its influence on smoothing motor movement, it is highly connected to regions of the limbic system and particularly regions associated with reward-based behavior. The nucleus accumbens, ventral pallidum, and ventral tegmental areas of the basal ganglia use dopamine to signal reward. Many stimulatory drugs with addictive qualities (e.g., cocaine, methamphetamine, nicotine) target this area.
Most PD cases are sporadic rather than familial and occur because of environmental factors or a combination of multiple genetic and/or environmental factors. Up to 15% of PD cases are found to be linked to genetic mutations, especially in early-onset PD (Gandhi et al., 2009). Multiple genetic mutations have been associated with PD, including the leucine-rich repeat kinase 2 (LRRK2), PARK2, SNCA, PARK7, and PINK1 genes.
Mutations in the LRRK2 gene have been associated with late-onset PD, which occurs after the age of 50 years (Nuytemans, Theuns, Cruts, & Van Broeckhoven, 2010). The LRRK2 gene codes for a multidomain protein known as dardarin, which has been linked to play an integral role in signaling pathways that are significant for neuron tunctioning as well as protein-protein signaling (Nuytemans et al., 2010). Mutations in the LRRK2 gene affect the dardarin protein structure and function. Some work has shown that the mutant form of dardarin induces apoptosis and interacts with parkin contributing to cytosolic protein aggregation (Smith et al., 2005). LRRK2 mutations do result in abnormal protein degradation and protein aggregation (Lesage & Brice, 2009). Increased aggregation of cytosolic proteins may contribute to apoptosis leading to the movement and balance dysfunction found in PD; however, specific mechanisms remain unknown (Gandhi et al., 2009).
The PARK2 gene codes for a protein called parkin, which is hypothesized to target proteins for enzymatic degradation. Parkin is also linked to the degradation of dysfunctional mitochondria. Mutations in the PARK2 gene have been linked to early-onset (juvenile) or autosomal recessive PD (Nuytemans et al., 2010). Because of these mutations, the parkin protein is dysfunctional, and research suggests that this loss of normal parkin activity leads to an accumulation of the unwanted proteins, which may interrupt normal cell activities, including release of dopamine (Tan & Skipper, 2007). Because parkin is generally abundant in the CNS, the dysfunction of parkin may lead to a loss of dopaminergic neurons, which may then result in the characteristic symptoms of PD (Gandhi et al., 2009). Studies have also shown that PARK2 mutations may be linked to decreased mitochondrial activity as well as heightened vulnerability to mitochondrial toxins, and if the mitochondria is affected in dopaminergic neurons, it may affect dopamine transmission, leading to PD signs and symptoms (Nuytemans et al., 2010).
The SNCA gene codes for making the alpha-synuclein protein, which is found within neurons at presynaptic nerves and in other cell types. Alpha-synuclein plays a crucial role in neurotransmission because it regulates the amount and release of synaptic vesicles, which contain important neurotransmitters like dopamine (Recchia et al., 2004). Mutations in the SNCA gene may lead to an accumulation of the alpha-synuclein protein, which then leads to an abnormal buildup of dopamine. The body then breaks down what is sensed to be "excess" dopamine, leading to neuronal cell death and the characteristic signs and symptoms of PD (Recchia et al., 2004).
The PARK7 gene codes for the PARK7 protein, also called DJ-1. This protein plays multiple roles in the body; DJ-1 acts as an antioxidant, protecting neurons from oxidative stress, and has also been linked to prevent accumulation of alpha-synuclein (Tan & Skipper, 2007). Mutations in the PARK7 gene lead to dysfunction of the DJ-f protein, which leads to aggregation of alphasy-nuclein, leading to the buildup and degradation of excess dopamine (Tan & Skipper, 2007). Dysfunction of DJ-1 also leads to oxidative stress, which leads to dopaminergic neuronal death. The resulting loss of dopamine in both these cases may be what leads to the signs and symptoms of PD (Nuytemans et al., 2010).
Another gene mutation that may play a role in causing signs and symptoms of PD is the PINK1 gene mutation. PINK1 mutations are associated with autosomal recessive, early-onset PD (Hilker et al., 2012). The PINK1 gene codes for a protein, PTEN, which is found in the mitochondria of cells throughout the body. The protein, PTEN, is thought to play a protective role in response to oxidative stress (Nuytemans et al., 2010). Normal PTEN protein inhibits apoptosis; the PTEN protein resulting from mutation of the PINK1 gene does not and may therefore contribute to increased neuronal cell death.
Not only are there genetic links, there are also environmental and toxin exposures that have been linked to PD. One such environmental link is a neurotoxin known as MPTP (l-methyl-4-phenyl-l,2,3,6-tetrahydropyridine; Smeyne & Jackson-Lewis, 2005). A number of drug users presented with symptoms of PD after injecting themselves with illegal narcotics contaminated with the neurotoxin MPTP. This led to research exploring the role of MPTP, and it was determined that the neurotoxin destroyed the dopaminergic neurons, leading to permanent symptoms similar to that of PD (Smeyne & Jackson Lewis, 2005).
Another reported environmental toxin that has been linked to symptoms of PD is rotenone, a chemical that is used as a broad-spectrum pesticide and insecticide (Franco, Li, Rodriguez-Rocha, Bums, & Panayiotidis, 2010). Although further research is needed to determine the exact correlation between this toxin and PD, previous animal research showed that injection of this chemical toxin resulted in these rats developing symptoms similar to that of PD (Franco et al., 2010). Although there is no definitive link between environmental toxins and development of PD, it is hypothesized that increased exposure to such toxins increases the likelihood of developing PD.
In summary, PD has been linked to genetic mutations, environmental toxins, or a combination of the two. Aging is also an identified risk factor. However, genetic mutations, environmental toxins, and aging are factors that account for less than 15% of all PD cases; the remaining cases are idiopathic. Scientists continue to research in the hopes of understanding the exact progression of events that lead to the depletion of dopamine.
PD is hallmarked by loss of dopaminergic neurons of the substantia nigra, which are vital for fluid and smooth motor movement. Dopaminergic stimulation increases direct pathway excitation and decreases indirect pathway inhibition. Loss of these dopaminergic neurons leads to an imbalance between excitation and inhibition (Bergman & Deuschl, 2002). Specifically, there is an increased excitation of the indirect pathway (and inhibition) rather than a balance between both indirect and direct pathways. The increased stimulation of the indirect pathway causes increased inhibition of neurons in the thalamus, thus leading to increased inhibition of motor neurons in the cortex. The resulting effect is an overall decrease in motor function (Rodriguez-Oroz et al., 2009). The specific cause or mechanism of substantia nigra cell loss in PD is not understood.
Not only is depletion of dopaminergic neurons of the substantia nigra seen in PD, there are also Lewy bodies present, which are abnormal protein inclusions (Schulz-Schaeffer, 2010). Lewy bodies are insoluble protein aggregates that are primarily made up of a-synuclein fibers and, often, other abnormal proteins in the cytosol of neurons (Schulz-Schaeffer, 2010). In PD, Lewy bodies are mainly found in the substantia nigra. Early in disease development, Lewy bodies are also present in the olfactory bulb, medulla oblongata, and certain regions of the pons that regulate sleep (Ballard, Kahn, & Corbett, 2011). Later in PD progression, Lewy bodies present in the substantia nigra and the neocortex (Schulz-Schaeffer, 2010). Although the presence of Lewy bodies is one of the main pathologic indicators of PD, there are many questions still to be answered regarding Lewy bodies and their association with dopaminergic neurodegeneration and with the symptoms of PD (Schulz-Schaeffer, 2010). It is not clear if Lewy bodies promote neuronal degeneration, are simply a by-product of neuronal dysfunction/degeneration, or perhaps, may be protective and signal efforts to preserve individual brain cells (Schulz-Schaeffer, 2010).
There is still much to be discovered regarding the pathophysiology of cognitive impairment associated with PD. However, many published research studies link cognitive manifestations of PD, particularly dementia, to the presence of SNCA-positive Lewy bodies. The amount of Lewy bodies in patients with PD and dementia is found to be significantly higher than in those with PD without dementia (Williams-Gray, Foltynie, Lewis, & Barker, 2006). Other research suggests a stronger association between cognitive impairment of PD and Lewy body distribution, rather than the amount, within the cerebral cortex (Williams-Gray et al., 2006).
Signs and Symptoms
Symptoms of PD are not typically seen until there is up to 80% loss of dopaminergic neurons (Rodriguez-Oroz et al., 2009). Normally, impulses are "dampened" to create smooth and coordinated movements, in which some impulses are inhibited and some are facilitated. However, when major loss of dopaminergic neuron function occurs in PD, more and more impulses are facilitated, leading to the four cardinal symptoms of PD: tremor, bradykinesia, rigidity, and postural instability (Jankovic, 2008).
The most common symptom of PD is tremor at rest. Tremors in PD usually occur in distal portions of the limbs and can present as "pill-rolling" tremors in the hands as well as tremors in the legs, chin, lips, and even jaw (Jankovic, 2008). These tremors occur at rest but usually cease when actions are performed as well as during sleep. How exactly this tremor occurs in relation to the dopaminergic loss in patients with PD is not clearly understood (Rodriguez-Oroz et al., 2009). Some scientists surmise that the loss of dopaminergic neurons leads to an imbalance between excitatory and inhibitory neurotransmissions and, in turn, the cerebral cortex fails to carry out fine movements. Others hypothesize that the deficiency of other neurotransmitters may play a role in causing tremors in PD, including serotonergic cells (Bergman & Deuschl, 2002).
Bradykinesia is also another major symptom of PD. Defined as the slowness of movement, bradykinesia is presented in PD as difficulty or slowness in the initiation of and carrying out movements (Jankovic, 2008). There is also slowness in carrying out several tasks at one time as well as slower reaction time. It is hypothesized that bradykinesia is linked to the depletion of dopaminergic neurons in the substantia nigra/pars compacta; the slowness in movement that occurs is because of an interference in the motor cortex pathway, caused by the significant loss of functioning dopaminergic cells (Jankovic, 2008). Consequently, patients with PD must exert a substantially greater amount of effort in the initiation and execution of movements.
The third major symptom of PD is muscle rigidity. Although muscle rigidity is considered a characteristic symptom of PD, the pathophysiology relating to dopaminergic loss and how it leads to muscle rigidity has not been established (Jankovic, 2008). The patient experiences increased resistance in the shoulders, neck, wrists, hips, and so forth. Rigidity may occur in both the flexor and extensor muscles; however, the flexor muscular sets are heavily affected as PD progresses (Rodriguez-Oroz et al., 2009). Voluntary movement of the areas will typically greatly increase the rigidity even more and may also be accompanied with pain (Jankovic, 2008).
The fourth cardinal symptom of PD is postural instability, which is related to rigidity. Postural instability is characterized as a loss of balance because of loss of postural reflexes (Jankovic, 2008). Researchers suggest that the disruption of the motor cortical pathways by dopamine depletion may play a role in causing the loss of postural reflexes and, consequently, postural instability (Rodriguez-Oroz et al, 2009). Postural instability is typically seen in the late stages of the disease and is known to be a great risk factor for falls and fractures in patients with PD (Jankovic, 2008).
There are several other symptoms common to PD. A mask-like facial expression, speech problems, and swallowing problems are common motor symptoms (Jankovic, 2008). Nonmotor impulses are also modified by the substantia nigra. Loss of dopaminergic neurons thereby contributes to a wide variety of nonmotor symptoms (Jankovic, 2008). Autonomic nervous system dysfunction, hallmarked by orthostatic hypotension, urinary incontinences, sweating, oily skin, and gastrointestinal problems, is common to patients with PD (Caballol, Marti, & Tolosa, 2007). Vision disturbances, dry eyes, saccadic eye movements, impaired sensations such as paresthesia, impaired pain sense, and impaired olfactory function are all altered in PD as well (Caballol et al., 2007). The neuropsychiatric dysfunction associated with PD is less well understood. These include mood disorders, cognitive impairment, dementia, behavioral disorders, and psychoses (Caballol et al., 2007). Sleep disturbances are also common (Jankovic, 2008).
Because symptoms of PD are not typically seen until major dopaminergic function is lost, it is difficult to recognize and intervene with medical management in the early progress of the disease. However, there are currently successful modes of treatment in place to help patients cope with the disease and the symptoms.
Levodopa (L-dopa, Dopar, Larodopa) is considered to be the main mode of treatment of PD. Levodopa is a precursor to dopamine and is used as treatment, rather than dopamine itself, because levodopa is able to cross the blood-brain barrier. Although it is able to cross the blood-brain barrier, levodopa is still metabolized by enzymes (Hristova & Roller, 2000); to minimize this metabolism and breakdown of synthetic levodopa, carbidopa is often given in combination. Carbidopa (Lodosyn) is an aromatic-L-amino-acid decarboxylase inhibitor. Inhibition of this enzyme prevents the breakdown of levodopa to dopamine in the body, thereby inhibiting levodopa metabolism promoting normal levels in the CNS (Muller, 2013). Once levodopa enters the CNS, it is converted to dopamine so that there is replacement of the breakdown of dopamine in the substantia nigra and other areas of the brain, resulting in increased amount of dopamine at the neuronal presynapse (Muller, 2013). Increased presynaptic dopamine restores some of the effects of substantia nigra cell loss, leading to increased smooth and coordinated movement through the direct and indirect pathways in the dopamine neurotransmitter system.
There are several side effects of levodopa-carbidopa (Sinemet, Parcopa, Atamet). One major effect is the gradual development of adverse motor effects such as dyskinesia, which may not appear until 2-5 years after beginning levodopa-carbidopa (Muller, 2013). Other side effects of levodopa-carbidopa include nausea or vomiting, orthostatic hypotension, agitation, hallucinations, dizziness, confusion, and clenching or grinding of the teeth (Hristova & Roller, 2000).
Studies suggest that long-term use of levodopa may in fact decrease the effectiveness of the medication and is associated with fluctuations in motor function because of the wearing-off effect and the adverse effect of dyskinesia (Muller, 2013). For this reason, some physicians choose to prescribe their patients with PD a sustained-release version of levodopa or may instruct their patients to decrease the frequency of intake of levodopa to maintain maximum efficiency (Hristova & Roller, 2000).
Another group of medications that can be used to symptomatically treat PD is dopamine agonists (DAs). DAs, such as ropinirole (Requip, Repreve, Ronirol, Adartel) and pramipexole (Mirapex, Mirapexin, Sifrol), are chemicals that act on the postsynaptic terminals within the striatum and activate the postsynaptic receptors to reduce dopamine turnover (Hristova & Roller, 2000). In doing so, DAs are able to increase available dopamine within the synapse and provide some moderate relief of symptoms of PD. Side effects of such medications include hallucinations, somnolence, impulse control disorders, and edema. However, there is decreased incidence of dyskinesia with the use of DAs (Hristova & Roller, 2000).
Medications such as levodopa-carbidopa and DAs help to provide symptomatic relief and delay the progression of PD but are not effective indefinitely. The disease does continue to progress, and patients may eventually develop cognitive or psychiatric deficits such as dementia and depression and long-term motor complications such as postural instability and dyskinesia (Hristova & Roller, 2000).
There has also been research conducted on nonpharmacologic management of PD, namely, exercise and rehabilitative methods such as physical therapy, occupational therapy, and even speech therapy (Post, van der Eijk, Munneke, & Bloem, 2011). These methods aim to maximize motor function, as well as quality of life, for as long as possible and to slow the progression of the symptoms of PD by educating patients on how to compensate for the loss of fine motor control they have over their uncoordinated movements (Post et al., 2011).
It is especially important to use a multidisciplinary approach to both nonpharmacologic management and pharmacologic treatment of patients with PD, utilizing healthcare professionals such as the nurse, neurologist, occupational therapist, speech therapist, dietician, psychologist, and others. Research has shown that involving the whole healthcare team in the patient's therapy and symptom management plan is correlated with improvement in not only the patient's motor control but also his or her overall quality of life (Post et al., 2011).
Summary and Nursing Implications
PD is a progressive disease caused by dopaminergic neuron loss within the substantia nigra. The cause of PD is unknown but is likely multifactorial with both genetic and environmental influences. The main symptoms of PD are tremor, bradykinesia, rigidity, and postural instability. Eventually, PD progresses to interfere with activities of daily living. Although there is no current cure for PD, patients with the disease are symptomatically managed through both pharmacologic and rehabilitative therapies.
Modern therapies and continuous research aim to evaluate the pathophysiology of PD and manage symptoms so that patients with the disease are living longer with increased quality of life. However, it is the role of the nurse to provide patients with PD the best possible care while struggling with such a complex, multifaceted disease; nurses are able to individually guide and tailor patients' care regarding multidrag therapies, coping mechanisms, and adjusting to life with motor dysfunction as well as emotional support for both the patient and the family throughout the course of the disease. It is the nurse's responsibility to collaborate with other members of the interdisciplinary healthcare team to best meet the needs of the patient with PD. Clinical nurses are a vital part of the healthcare team and work alongside doctors, advanced practice nurses, and pharmacists to tailor medication schedules and minimize PD symptoms and side effects while maximizing symptom relief; nurses have the power to take initiative and work with physical and occupational therapists to improve motor function and tailor exercises that best meet the patients' needs; and nurses are also able to work with specialized nutritionists and dieticians and assess patients with PD in not only their ability to physically eat but also how their nutritional status affects their symptoms and overall health status. These are just few examples of how nurses are able to provide quality care for patients with PD.
Nurses follow patients with PD on a more intimate level in that they are able to recognize even slight changes in individual patient function; they think critically and provide feedback and suggestions to other members of the healthcare team on changes in medication regimen, respiratory treatments, physical therapy, nutrition and diet, communication skills, and many more aspects that affect the patient's quality of life. Nurses are truly change agents and are often responsible for initiating and exploring new research opportunities to improve quality of life with PD. A clear understanding of the underlying pathophysiology of PD, its relationship to symptoms, and how it is modified by treatments is vital to the nurse contributing to the multidisciplinary care planning for patients with PD. By understanding the physiologic dysfunction of PD and its management, they are best able to provide the best possible care for patients with PD, collaborate with other members of the healthcare profession, initiate and implement pioneer clinical interventions, and have the incredible opportunity to institute changes in care to maximize individual patient outcomes and see direct results of that care.
Questions or comments about this article may be directed to Sheila A. Alexander, RN PhD, at firstname.lastname@example.org. She is an Associate Professor, Acute and Tertiary Care, School of Nursing, and Critical Care Medicine, School of Medicine, University of Pittsburgh, Pittsburgh, PA.
Apoorva Gopalakrishna, BSN, Student, University of Pittsburgh School of Nursing, Pittsburgh, PA.
The authors declare no conflicts of interest.
Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal's Web site (www.jnnonline.com).
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|Title Annotation:||Clinical Nursing Focus|
|Author:||Gopalakrishna, Apoorva; Alexander, Sheila A.|
|Publication:||Journal of Neuroscience Nursing|
|Date:||Dec 1, 2015|
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