About this course:
The purpose of this activity is to enable learners to increase their general knowledge of Parkinson's disease and understand the medical and nursing management of affected patients.
Parkinson's Disease for APRNs
The purpose of this activity is to enable learners to increase their general knowledge of Parkinson's disease and understand the medical and nursing management of affected patients.
Upon completion of this activity, participants should be able to:
- describe pathophysiological changes that occur in Parkinson's disease
- list proposed risk factors for Parkinson's disease
- describe the clinical manifestations associated with Parkinson's disease
- describe the pharmacological management of symptoms of Parkinson's disease
- discuss nursing care aimed at managing/controlling symptoms, promoting independence, and dealing with the chronicity of the disease
Parkinson's disease (PD) is a degenerative neurological disorder that results in alterations in balance, coordination, and movement (Bauldoff et al., 2020; National Institute on Aging, 2022). This disease has far-reaching impacts on quality of life and is increasing in prevalence. PD is the second most common type of neurodegenerative disease (MacMahon et al., 2021). According to the Parkinson's Foundation (2022), one million Americans live with PD; this number is expected to increase to 1.2 million by 2030. The onset of the disease is typically after the age of 60; however, 5%–10% of individuals will be diagnosed with young-onset PD before the age of 50 (National Institute on Aging, 2022).
Anatomy and Physiology
Movement is facilitated by the basal ganglia, which is a group of neurons located beneath the cerebral cortex (Britannica, 2022). Through the release of neurotransmitters, motor neurons give and receive signals that promote the movement of skeletal muscles (American Association of Neurological Surgeons [AANS], 2022a). The basal ganglia, in coordination with the cerebellum, regulate motor movement by sending information through the thalamus to the cerebral cortex. The signals coming from the basal ganglia are inhibitory, while the signals coming from the cerebellum are excitatory. Coordination of movement is accomplished through a balance between both systems (Hoffman & Sullivan, 2017).
More specifically, the neurotransmitter dopamine is responsible for movement. Dopamine binds to G-protein-coupled receptors to promote motor control, cognitive function, motivation, and reward. Imbalances in dopamine impact muscle coordination (Klein et al., 2019).
In individuals experiencing PD, the basal ganglia deteriorate, and dopamine levels are low (Norris, 2019). Specifically, a drop in circulating dopamine is a result of the destruction of neuronal cells in the substantia nigra located in the basal ganglia of the brain (Honan, 2019; MacMahon et al., 2021). The dopaminergic nigrostriatal pathway degenerates, causing an imbalance of neurotransmitters in the corpus striatum (Norris, 2019).
Typically, the neurotransmitters acetylcholine (excitatory) and dopamine (inhibitory) counterbalance each other when relaying impulses to the higher motor centers of the brain. As a result, motor movement is controlled and refined (Hinkle & Cheever, 2018; Honan, 2019). When there is a loss of neuronal cells in the substantia nigra of the basal ganglia, dopamine storage is depleted. This provokes a predominance of the excitatory neurotransmitter acetylcholine over the inhibitory neurotransmitter dopamine. The ability to fall and stay asleep is affected by increased acetylcholine levels, and muscle rigidity makes changing positions during sleep difficult (Bauldoff et al., 2020). Clinical manifestations of PD become apparent when approximately 60% of the neuronal cells in the substantia nigra are destroyed, and the dopamine level is decreased by 80% (Hinkle & Cheever, 2018; Honan, 2019).
Risk Factors and Protective Features
Men are diagnosed with PD more often than women. Advancing age, genetics, head trauma, and exposure to toxins are also risk factors for an individual to develop PD (Norris, 2019). Oxidative stress caused by toxins promotes protein aggregation, neuroinflammation, microglial cell activation, and mitochondrial dysfunction, all of which promote neuronal death (Agnihotri & Aruoma, 2020).
Signs and Symptoms
The clinical manifestations of PD progress slowly (Hinkle & Cheever, 2018; Honan, 2019). Cardinal signs of PD can be recalled through the mnemonic TRAP, which stands for:
- rigidity of muscles
- postural disturbances (Honan, 2019)
Most patients present with a slow, unilateral, resting tremor at the time of diagnosis. A resting tremor occurs while the extremity is motionless and disappears with purposeful movement (Hinkle & Cheever, 2018; Honan, 2019). This tremor can involve a rhythmic, slow-turning motion of the forearm and hand (pronation to supination) accompanied by movement of the thumb against the other fingers as if rolling a pill (Honan, 2019). As the disease progresses, the tremor may become bilateral and affect the patient's ability to perform activities that require dexterity, such as eating and writing (Bauldoff et al., 2020).
Rigidity manifests as passive resistance to limb movement. The passive range of motion of an extremity can result in a jerky movement known as cogwheel rigidity. An early manifestation of rigidity is cramping in the hands or toes or shoulder pain. Patients may also report stiffness, heaviness, or muscle aches due to rigidity (Bauldoff et al., 2020; Honan, 2019).
Akinesia and Bradykinesia
Akinesia is a lack of movement, while bradykinesia is a delay in the execution of movement (Honan, 2019). Patients may have difficulty initiating actions such as rising from a chair or changing positions in bed (Hinkle & Cheever, 2018).
Patients with PD experience a loss of postural reflexes (Honan, 2019). An involuntary flexion of the head and shoulders results in an inability to maintain the trunk in an upright position while sitting or standing (Bauldoff et al., 2020). As the patient attempts to move their feet under the body's center of gravity, they demonstrate a shuffling gait with decreased arm swing (Honan, 2019). Additionally, patients with PD have difficulty with pivoting, which can impair balance and result in falls (Bauldoff et al., 2020).
Other Signs and Symptoms
Some symptoms of PD result from a loss of functions controlled by the autonomic nervous system (Bauldoff et al., 2020). This includes excessive and uncontrolled sweating, paroxysmal flushing, elimination problems (e.g., constipation and urinary hesitancy or frequency), orthostatic hypotension, and sexual dysfunction, including erectile dysfunction, decreased libido, vaginal dryness, and anorgasmia (Bauldoff et al., 2020; Honan, 2019; Wright, 2019). Due to increased sweat gland activity, patients may experience eczematous skin changes and seborrhea (Bauldoff et al., 2020).
In many instances, PD patients will also develop dysphagia, posing a risk for aspiration. Dysphonia (a soft, low-pitched, nasal-sounding voice) can also occur in response to muscle weakness associated with speech and paralysis of the soft palate. As dexterity declines, patients develop micrographia (small, shrinking handwriting; Honan, 2019). The face also appears mask-like (i.e., expressionless), and blinking decreases (Hinkle & Cheever, 2018; Honan, 2019).
Patients with PD also report sleep
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A diagnosis of PD should be confirmed by a neurologist after a thorough neurological examination with disease staging. Careful assessment is needed, as PD signs and symptoms mimic other disease processes (National Institute on Aging, 2022). The gold-standard staging assessment uses the 4-part Movement Disorder Society – Unified PD Rating Scale (MDS-UPDRS), which examines non-motor experiences of daily living, motor experiences of daily living, motor function, and motor complications—specifically, motor complications that are specific to parkinsonism symptoms, such as bradykinesia, a resting tremor, and muscle rigidity. The section on non-motor aspects asks the patient (or caregiver) about sleep disturbances, discomfort, urinary control, constipation, lightheadedness, and fatigue. The motor aspects include problems with speech, drooling, swallowing, feeding/eating, dressing, hygiene, handwriting, participating in hobbies, turning over in bed, a tremor, transitioning from sitting to standing, walking/balance, freezing (i.e., a brief period of immobility with a sensation of suddenly being unable to move). The motor function section requires the examiner to rate the patient's speech, facial expressions, rigidity, finger tapping, hand opening/closing, hand pronation/supination, toe tapping, foot stomping, rising from a chair, walking/gait, postural stability, posture, body bradykinesia (i.e., global spontaneity of movement), hand tremors (postural, kinetic, resting, constancy). The final section assesses motor complications. It specifically investigates the presence of dyskinesias (i.e., involuntary random movements), dystonias (i.e., contorted posture with a twisting component), and motor fluctuation (i.e., the variable response to medication or on-off effect). It asks for separate ratings regarding time spent in these states as well as their functional impact. All items are given a score rating between 0 (no observable or reported symptoms) and 4 (severe symptoms). The total score for each section is obtained, but a total overall score is not clinically relevant (Chou, 2022; Goetz et al., 2008; Postuma et al., 2015).
The clinical (and research) criteria published by the Movement Disorder Society (Postuma et al., 2015) dictate that parkinsonism must be established first. This requires the presence of observable bradykinesia and either a resting tremor or rigidity. Clinical diagnosis is then established, assuming there are no red flags or absolute exclusion criteria and at least two supportive criteria. If one or two red flags exist and are counterbalanced by one to two supportive criteria, then the diagnosis is considered probable. Red flags, exclusion criteria, and supportive criteria can be found in Table 1 (Chou, 2022; Postuma et al., 2015).
Red Flags, Exclusion Criteria, and Supportive Criteria for Parkinson's Disease
Exclusion criteria (their presence rules out a diagnosis of PD)
In addition, neurologists rarely use imaging and diagnostic tests to confirm a diagnosis of PD, such as computerized tomography (CT) scanning, genetic testing, magnetic resonance imaging (MRI), and positron emission tomography (PET; Belloli et al., 2020; Pagano et al., 2016). Other studies include a sleep study and dopamine transporter scanning (DaTscan). The sleep study identifies whether an individual acts out their dreams, while the DaTscan examines changes in dopamine levels in the brain via a gamma camera (Oregon Health & Science University Brain Institute, 2022).
The most common underlying etiology of tremor is essential tremor, with the distinguishing feature that essential tremors are typically bilateral, symmetric, and worsen with action or intention of action. The tremor seen with PD is most often a resting tremor that resolves with action, especially in early disease. Scans without evidence of dopaminergic deficit (SWEDD) are patients with isolated upper extremity tremors that do not progress into generalized PD; these represent roughly 10% of the patients with parkinsonism. Dementia with Lewy bodies is a form of dementia that is also characterized by rapid eye movement sleep disturbance and parkinsonism. Other conditions that may be ruled out when evaluating a patient for suspected Parkinson's Disease include:
- multiple system atrophy (MSA, previously olivopontocerebellar atrophy, striatonigral degeneration, and Shy-Drager syndromes)
- corticobasal degeneration
- progressive supranuclear palsy
- idiopathic familial basal ganglia calcification
- drug-induced parkinsonism
- vascular parkinsonism
- Huntington's disease
- frontotemporal dementia with parkinsonism
- spinocerebellar ataxia
- dentatorubral pallidoluysian atrophy
- secondary parkinsonism of alternative etiology (e.g., toxin exposure, head trauma, structural brain lesion, metabolic disorder, or infection; Chou, 2022).
Treatment and Management
Pharmacological management should be initiated when PD is identified and quality of life begins to decline. The decision to incorporate medication is mediated by a discussion between a neurologist and their patient. The goal of pharmacological therapy is to control the client's symptoms to the greatest possible extent. Considerations to include in the conversation are the effect of the disease on the dominant hand; the degree of interference in work, activities of daily living (ADLs), and social/leisure function; the presence of significant gait disturbance or bradykinesia; and patient preference (Bauldoff et al., 2020; Hoffman & Sullivan, 2017; Spindler & Tarsy, 2021). The medications discussed below are administered orally unless otherwise indicated.
Levodopa is converted to dopamine in the central nervous system. Carbidopa, a decarboxylase inhibitor, prevents the premature breakdown of levodopa to dopamine in the peripheral tissues. Carbidopa/levodopa (Parcopa, Sinemet) can relieve tremors and rigidity; it is considered the most effective treatment for PD symptoms (American Parkinson Disease Association, 2022a; Bauldoff et al., 2020; Vallerand, 2017). It is the preferred pharmacological treatment for moderate or severe Parkinson's but also requires the most frequent dosing (Spindler & Tarsy, 2021). Side effects of carbidopa/levodopa (Parcopa, Sinemet) include nausea, vomiting, constipation, decreased appetite, somnolence, headache, orthostatic hypotension, darkening of urine and sweat, and dyskinesias. Contraindications include angle-closure glaucoma and malignant melanoma (Hinkle & Cheever, 2018; Vallerand, 2017). Nausea may improve with increased carbidopa dosage or the addition of ondansetron (Zofran) or trimethobenzamide (Tigan). Orthostasis may be improved by discontinuing or reducing the dose of concurrent antihypertensive medications. Salt and water consumption can be increased, and abdominal binders or compression stockings can be worn (Spindler & Tarsy, 2021).
Many patients (at least 50%) develop levodopa-related complications within several (5-10) years of treatment. The risk of motor complications is the highest with levodopa, although motor complications are also seen with other oral anti-parkinsonism treatments. Patients may experience dyskinesias and an "on-off syndrome," which is characterized by periods of immobility (off effect) followed by a sudden return of mobility (on effect). This is most likely due to the progressive deterioration of dopamine terminals, affecting the uptake and release of dopamine and causing decreased buffering of plasma levodopa level fluctuations. This is directly related to levodopa's short (90-minute) half-life. Changing the dosing regimen or switching to another medication may help minimize this syndrome, as well as reducing the ingestion of protein before or with levodopa dosages. Extended-release (ER) formulations of levodopa (Rytary) may also lead to a reduced number of daily doses and, therefore, motor fluctuations, but at a higher cost (Liang & Tarsy, 2022; Spindler & Tarsy, 2021). Historically, clinicians would recommend that patients avoid initiating treatment with levodopa until symptoms significantly impact daily function. However, more recent evidence indicates that motor fluctuations and dyskinesia is more likely related to the change in pharmacodynamics as the underlying disease naturally progresses. This suggests that the timing of initial therapy has little impact on the long-term development of these motor complications. Instead, treatment should be initiated using the smallest effective dose to adequately manage symptoms (Hinkle & Cheever, 2018; Spindler & Tarsy, 2021).
Carbidopa/levodopa should be started using the IR formulation at 25/100 mg, one-half tab BID or TID with meals to limit nausea. This can be carefully titrated up over several weeks to a full tab TID with meals. The total dose should be titrated to a useful clinical response, which is typically 300-600 mg daily. Large-amplitude tremors may be treatment resistant with levodopa, but a lack of response to 1000-1500 mg of levodopa daily should prompt consideration of alternative underlying etiologies. Controlled release (CR) tablets can be started once dosing has been established in those desiring BID dosing. CR tablets are absorbed less efficiently and typically require up to 30% higher doses for an equivalent effect. Levodopa should always be tapered slowly when discontinuing. Sudden withdrawal can lead to neuroleptic malignant-like syndrome or akinetic crisis (Spindler & Tarsy, 2021).
When educating patients and families, the APRN should discuss rising slowly from a supine or seated position due to the risk for orthostatic hypotension; dividing daily protein intake among all meals, as high-protein meals can impair the medication's effectiveness; and adhering to all instructions for laboratory testing (liver function studies, renal function studies, and complete blood count with differential; Vallerand, 2017).
Dopamine agonists—such as pramipexole (Mirapex), ropinirole hydrochloride (Requip), and rotigotine (Neupro)—are useful in postponing the use of carbidopa/levodopa (Parcopa, Sinemet) therapy, or they can be used concurrently. Dopamine agonists mimic the role of dopamine in the brain and consequently decrease tremor and rigidity. Side effects consist of orthostatic hypotension, nausea/vomiting, somnolence, confusion, and psychologic disturbances such as hallucinations and impulse control disorders. They are of moderate potency and, therefore, slightly less effective at controlling motor symptoms than levodopa. They also carry a risk for motor complications as described above, but slightly lower risk than levodopa. They are typically not well tolerated by older adults and those with cognitive dysfunction. Contraindications for dopamine agonists include psychotic disorders. They are considered a reliable option in patients under 65 with moderate symptoms affecting their daily life and should be discussed with patients individually to determine if levodopa or a dopamine agonist is a better fit. In patients over 65, they are not as effective or as well tolerated as levodopa and are traditionally not optimal (Honan, 2019; Bauldoff et al., 2020; Spindler & Tarsy, 2021; Vallerand, 2017).
Pramipexole (Mirapex) is typically dosed at 0.125 mg TID initially and increased by 0.125 mg per dose every week. The ER formulation is started at 0.375 mg QHS and increased by 0.375 mg weekly. Most patients are managed with 1.5-4.5 mg daily. Doses should be reduced in patients with renal insufficiency. Ropinirole (Requip) is typically dosed at 0.25 mg TID initially and increased weekly by 0.25 mg per dose to a goal of 1 mg TID. The dose may then be increased to a maximum of 24 mg daily by increasing the dose by 1.5 mg weekly. The ER formulation is typically started at 2 mg QHS and titrated weekly in 2 mg increments. Most patients find maximum benefit from 12-16 mg daily. Rotigotine (Neupro) is available in a daily transdermal patch that is started at 2 mg/day and increased weekly by 2 mg to a goal dose of 6 mg/day. Sudden withdrawal of dopamine agonists can lead to neuroleptic malignant-like syndrome or akinetic crisis, so they should always be tapered slowly (Spindler & Tarsy, 2021).
Ergot dopamine agonists, such as bromocriptine (Parlodel) and cabergoline (Dostinex), now play a very limited role in the treatment of PD due to rare but severe complications after long-term use. Pergolide and cabergoline are associated with cardiac, peritoneal, and pulmonary fibrosis and valvular disease. Pergolide is no longer available for use in the US. The evidence linking bromocriptine (Parlodel) to valvular heart disease and an increased risk of fibrosis was insufficient but could not be excluded. Daily doses should be limited to 30 mg, and they should not be used in patients with pre-existing valvular disease (Spindler & Tarsy, 2021).
When educating patients and families, the APRN should discuss rising slowly from a supine or seated position due to the risk for orthostatic hypotension and notifying the HCP of any new or increased gambling, sexual or other intense urges, or psychotic-like behavior (Vallerand, 2017).
Amantadine hydrochloride (Symmetrel) is often used in early PD to manage mild symptoms related to akinesia and tremors or as an adjunct with levodopa to manage motor fluctuations and dyskinesias. The incidence of side effects is low but can include mood changes, confusion, depression, hallucinations, orthostatic hypotension, heart failure, edema of the lower extremities, nausea, urinary retention, headaches, and visual changes (Bauldoff et al., 2020; Hinkle & Cheever, 2018; Honan, 2019). It may cause a blue skin discoloration referred to as livedo reticularis. It also causes insomnia or nightmares infrequently, which may be avoided by switching to morning dosing. Amantadine (Symmetrel) is considered only modestly effective, yet convenient and well-tolerated by most patients. It is believed to function by increasing dopamine release, decreasing its reuptake, stimulating dopamine receptors, and potentially creating a central anticholinergic effect. It is typically dosed using the immediate release formulation (Symmetrel) in early disease (100 mg BID to TID). The extended-release version (Osmolex ER, Gocovri) is more expensive; it is started at 129 mg daily, may be increased weekly up to 322 mg/day, and should be tapered slowly when discontinuing. It may be considered as monotherapy in younger patients or older adults with mild symptoms that are tremor-predominant (Spindler & Tarsy, 2021).
When educating patients and families, the APRN should discuss rising slowly from a supine or seated position due to the risk for orthostatic hypotension; monitoring for signs and symptoms of heart failure, such as sudden weight gain, edema, or difficulty breathing; and notifying the HCP if incomplete bladder emptying is suspected (Vallerand, 2017).
Monoamine Oxidase-B (MAO-B) Inhibitors
MAO-B inhibitors, such as rasagiline (Azilect) and selegiline (Eldepryl), inhibit dopamine breakdown. They can be combined with dopamine agonists to delay the use of carbidopa/levodopa (Parcopa, Sinemet) therapy. Side effects include dizziness, orthostatic hypotension, insomnia, nausea, dry mouth, headaches, and serotonin syndrome. They may also cause confusion and hallucinations. Selegiline (Eldepryl) is available as a transdermal patch in addition to an oral formulation (Bauldoff et al., 2020; Hinkle & Cheever, 2018; Vallerand, 2017). MAO-B inhibitors, like amantadine (Symmetrel), are considered only modestly effective yet well-tolerated and convenient to administer. For this reason, they are most often used in those with mild symptoms. Selegiline (Eldepryl) is most commonly dosed at 5 mg BID (morning and mid-day), although some may find benefit with just once-daily dosing. Rasagiline (Azilect) can be started at 0.5mg daily and increased to 1 mg daily if well-tolerated. Safinamide (Xadago) is often given concurrently with levodopa and started at 50 mg daily. It may be increased to 100 mg daily after 14 days if tolerated (Spindler & Tarsy, 2021).
When educating patients and families, the APRN should discuss rising slowly from a supine or seated position due to the risk of orthostatic hypotension and avoiding consumption of tyramine-containing foods (e.g., aged cheeses, fermented meats, beer, and ale) due to the risk for hypertensive crisis. In addition, patients should notify their HCP if they develop any signs of serotonin syndrome, such as mental status changes, autonomic instability, neuromuscular changes, and/or gastrointestinal symptoms (Vallerand, 2017).
Catechol-O-Methyltransferase (COMT) Inhibitors
COMT inhibitors block the function of catechol-O-methyltransferase, which is the enzyme responsible for metabolizing dopamine. Entacapone (Comtan) or tolcapone (Tasmar) are given in combination with carbidopa/levodopa (Parcopa, Sinemet), allowing for more levodopa to be converted to dopamine in the brain (Honan, 2019). This is typically intended to reduce the "off" time in patients experiencing motor fluctuations related to levodopa treatment (Liang & Tarsy, 2022). Side effects include nausea, constipation, diarrhea, abdominal pain, hepatotoxicity, back pain, blood in the urine, and orthostatic hypotension (Hinkle & Cheever, 2018; Vallerand, 2017).
When educating patients and families, the APRN should discuss rising slowly from a supine or seated position due to the risk for orthostatic hypotension; avoiding intake of alcohol; and adhering to HCP instructions for laboratory testing, such as liver function studies (Bauldoff et al., 2020; Vallerand, 2017).
Anticholinergic agents control tremors by counteracting the action of the neurotransmitter acetylcholine. In a healthy brain, dopamine and acetylcholine are electrochemically balanced. Because PD is characterized by dopamine depletion, anticholinergic medications improve parkinsonian symptoms. Trihexyphenidyl hydrochloride (Artane) and benztropine mesylate (Cogentin) are examples of anticholinergics used to treat PD. Anticholinergics reduce tremors but have almost no impact on bradykinesia or gait disturbances (Hinkle & Cheever, 2018; Honan, 2019; Vallerand, 2017). For this reason, they are most often utilized in younger patients (less than 65) with significant tremors but without bradykinesia or gait disturbance. Trihexyphenidyl hydrochloride (Artane) is typically started at 0.5 to 1 mg BID, increasing gradually to 2 mg TID (Spindler & Tarsy, 2021)
Side effects include blurred vision, flushing, constipation, a dry mouth, hypotension, urinary retention, and cognitive/memory impairment. Anticholinergics are contraindicated in patients with angle-closure glaucoma, and they should be used cautiously in patients with benign prostatic hypertrophy. They are also typically avoided in older patients or those with cognitive impairment. In addition to the oral form, benztropine mesylate (Cogentin) is available for intramuscular and intravenous administration for acute dystonia and drug-induced extrapyramidal reactions (Hinkle & Cheever, 2018; Honan, 2019; Spindler & Tarsy, 2021; Vallerand, 2017).
When educating patients and families, the APRN should discuss rinsing the mouth frequently and using sugarless gum or candy to decrease dry mouth and rising slowly from a supine or seated position due to the risk for orthostatic hypotension (Vallerand, 2017).
A physical therapist, an occupational therapist, a speech therapist, and a social worker should all be part of the interdisciplinary care team. Physical therapy can provide individualized exercises and activities to promote strength, flexibility, and mobility (Hoffman & Sullivan, 2017). Examples of beneficial exercises may include stretching (stretch-hold-release), range-of-motion exercises, and postural exercises. Physical therapists should also work with patients on safe walking techniques, such as walking erect with the feet separated (creating a wide base of support) and looking straight at the horizon (Hinkle & Cheever, 2018; Honan, 2019).
Occupational therapy provides strategies to promote maximal independence and optimize mental functioning (Hoffman & Sullivan, 2017). The therapist can recommend available adaptive or assistive devices to help with daily function. Occupational therapists can also evaluate each patient's needs in their home environment and suggest modifications (Honan, 2019).
Speech therapy should include a swallow evaluation, as swallowing difficulties are common in patients with PD. Swallowing problems can be due to poor head control, tongue tremors, delayed swallowing, an inability to form a food bolus, or disturbances in pharyngeal motility. A speech therapist can identify the specific swallowing issues and make appropriate dietary recommendations. The speech therapist can also design speech improvement exercises, as PD patients tend to have soft, monotonous speech (Honan, 2019). Patients should be encouraged to speak slowly, exaggerate their pronunciation of words, face the listener, and use short sentences (Hinkle & Cheever, 2018; Honan, 2019).
A social worker can connect patients and caregivers with support groups and helpful resources such as the American Parkinson Disease Association and the Parkinson's Foundation (Bauldoff et al., 2020).
For carefully selected patients who may have advanced tremors that are no longer responsive to medications or are impaired by dyskinesias associated with long-term use of carbidopa/levodopa (Parcopa, Sinemet), deep brain stimulation (DBS) may be considered (Bauldoff et al., 2020; Hinkle & Cheever, 2018). According to the AANS (2022b), candidates for DBS must have a decreased quality of life, symptoms despite medication, and adverse effects from the medication regimen. In addition to medications, non-surgical treatments should be utilized before surgical intervention (AANS, 2022b).
DBS involves the delivery of high-frequency electrical stimulation to targeted areas of the brain identified through a CT scan or an MRI (Honan, 2019). One or more electrodes are placed in either the globus pallidus or subthalamic nucleus and connected to a pulse generator via an extended wire. The battery-powered pacemaker is placed beneath the collarbone (AANS, 2022b; Hinkle & Cheever, 2018; Honan, 2019).
Stimulation to these areas may increase dopamine release, leading to a reduction in tremors and rigidity. The goal is for medication doses to decrease after the insertion of this device (Hinkle & Cheever, 2018). Individuals who have DBS may have the surgery bilaterally and experience continuous symptom management. The risks of surgery are as follows:
- brain hemorrhage (e.g., cerebral vascular accident)
- device malfunction
- persisting disease symptoms
- worsening emotional or mental status (AANS, 2022b)
Long-Term Outcomes for Surgical Management
Overall, DBS has demonstrated positive long-term outcomes in PD surgical candidates (Bove et al., 2021). Studying PD patients at the 3- and 5-year marks, Shin and colleagues (2020) found that levodopa medication dosages were decreased in all 49 patients who underwent DBS. Hitti and colleagues (2019) demonstrated that DBS was effective for long-term symptom management, highlighting a 51% survival rate at a 10-year telephone follow-up for 200 patients. The retrospective study included 320 patients who had DBS from 1999–2007. Similarly, Bove and colleagues (2021) found statistically significant improvement in 51 patients at a 15-year follow-up after DBS placement (p<0.001); these patients required fewer dopamine-replacement medications, reported greater quality of life, and experienced fewer dyskinesias.
Evidence-Based Nursing Practice
Changes in mobility reportedly decline within the first 5 years of PD diagnosis (Johansson et al., 2020). Therefore, educating patients on fall prevention and sustaining muscle strength is important. Daily exercise will help increase muscle strength, improve coordination, decrease muscle rigidity, and prevent contractures (Hinkle & Cheever, 2018). Walking, riding a stationary bicycle, and swimming can help maintain joint mobility (Honan, 2019). Using a treadmill or an elliptical machine can enhance gait, stride length, and speed (International Parkinson and Movement Disorder Society, 2018). Warm baths and massage help facilitate range-of-motion exercises (Hinkle & Cheever, 2018). Because patients with PD often lack a normal arm swing, APRNs should remind patients to make a conscious effort to swing their arms and pick up their feet while walking (e.g., by practicing walking to marching music; Honan, 2019).
Beneficial Non-Traditional Forms of Exercise
Besides walking, using traditional workout equipment, and swimming, non-traditional forms of exercise can help prevent falls in the PD population. APRNs can introduce these during patient education encounters. Tai chi improves posture control and balance, preventing falls (International Parkinson and Movement Disorder Society, 2018). Research by Li and colleagues (2020) on 500 individuals with early PD found that incorporating tai chi with traditional forms of exercise prevented falls and limited levodopa dosages more than traditional exercise alone (p<0.0001, q=38.512).
Pereira and colleagues (2019) examined 40 studies and 5 reviews on music and dance therapy for individuals with PD, finding that music and dance therapy enhanced motor ability, cognition, and quality of life. More specifically, the tango enhanced spatial awareness, the ability to focus, and coordination (Guettard et al., 2018; International Parkinson and Movement Disorder Society, 2018; Rabinovich et al., 2021). APRNs can recommend classes at a dance studio, senior center, or home-based programs.
Many individuals with PD experience weight loss and malnutrition (Ma et al., 2018). Each patient's weight should be monitored weekly to identify concerns (Hinkle & Cheever, 2018). Eating requires extra concentration due to chewing and swallowing difficulties, as well as the medication-related side effect of dry mouth (Hinkle & Cheever, 2018; Honan, 2019). Patients should sit in an upright position when eating to facilitate the swallow reflex and decrease the risk of aspiration (Hoffman & Sullivan, 2017). Suction equipment should be readily available at the bedside in the event of aspiration and to assist with handling oral secretions (Hoffman & Sullivan, 2017).
A semisolid diet with thickened liquids is easier to swallow, so recommendations from speech therapists may include avoiding thin liquids. The patient should place food on their tongue, close their lips and teeth, and lift the tongue up and then back to swallow. Patients should be encouraged to chew food first on one side and then the other before swallowing (Hinkle & Cheever, 2018; Honan, 2019).
To assist with eating and promote independence, a plate stabilizer, a no-spill cup, and built-up handles for utensils can be of value. APRNs may need to collaborate with occupational therapists to secure these devices if applicable. As PD progresses, patients may need a percutaneous endoscopic gastrostomy (PEG) tube to maintain adequate nutritional intake (Honan, 2019).
Cognitive-linguistic impairments are frequently overlooked in the clinical care of patients with PD (Smith & Caplan, 2018). Patients with PD may benefit from speaking slowly and deliberately and taking a few deep breaths (Hinkle & Cheever, 2018). An electronic amplifier may be useful if family members, caregivers, or providers are having difficulty hearing the patient (Honan, 2019).
Patients with PD are at risk for social isolation due to a decline in their abilities to communicate clearly (Theodoros et al., 2019). APRNs can refer patients to speech and language therapy. In addition, APRNs should also be mindful of patients' altered self-confidence and self-perception as their communication abilities change (Johansson et al., 2020).
Improving Bowel Elimination
PD may cause severe constipation from several factors. Weakening of the muscles used for defecation, immobility, decreased fluid intake due to impaired swallowing, decreased autonomic nervous system activity, and adverse effects of medications can all contribute to constipation. The following measures should be incorporated into the plan of care: setting a regular schedule for defecation, consuming foods with moderate fiber content, and increasing fluid intake. A raised toilet seat and allowing ample time for bowel movements may also be of benefit (Hinkle & Cheever, 2018). If nonpharmacological techniques are ineffective in managing constipation, providers can suggest various pharmacological agents, such as bulking agents, osmotic and stimulant laxatives, chloride channel activators, ghrelin agonists, 5-HT4 receptor agonists, and probiotics (Mozaffari et al., 2020).
Promoting Self-Care Activities
Modifications to the patient's environment can compensate for diminished abilities and promote safety and independence. APRNs should counsel patients to remove throw rugs, ensure sufficient lighting throughout the home, and install handrails in all bathrooms and stairwells (Honan, 2019). Occupational therapists can determine the best assistive devices for each patient. Additionally, APRNs should encourage patients and caregivers to manage their medication regimen carefully to promote balance and limit side effects.
Medications that treat PD can often contribute to sleep pattern disturbances. For example, levodopa (Parcopa, Sinemet) can lead to vivid dreams. In addition, many individuals experience insomnia, daytime sleepiness, and restless leg syndrome (Stefani & Högl, 2020). Sleep pattern hygiene basics include going to bed and waking around the same time every day, avoiding naps too close to bedtime, limiting caffeine intake, darkening the bedroom, and decreasing any ambient noise (American Academy of Sleep Medicine, 2020; Bauldoff et al., 2020). Patients with PD may require a video-polysomnography to identify changes in sleep patterns and guide other recommendations (Stefani & Högl, 2020).
Supporting Coping Abilities
Patients with PD often experience apathy, loneliness, and embarrassment about their external symptoms. These feelings can lead to depression and anxiety. APRNs can offer some strategies when appropriate to combat depression, such as achievable goals, physiotherapy, support group participation, medication therapy, and psychotherapy (Honan, 2019). Patients with PD have demonstrated positive results with cognitive behavioral therapy, including when provided over the telephone (Dobkin et al., 2020; Reynolds et al., 2020). If a patient expresses an interest in medication therapy for mood stabilization, APRNs should offer additional information. As always, APRNs should be watchful for any worsening mood symptoms or suicidality.
Future research includes looking at the presence of Lewy bodies, using stem-cell-based treatments, and understanding the impact of neuroinflammation on PD individuals.
Although there is no indication that Lewy bodies cause PD, researchers have noted their presence in brains affected by PD (Norris, 2019). Lewy bodies are alpha-synuclein proteins that clump in association with changes in cognition and motor function (American Parkinson Disease Association, 2022b). Most notably, Lewy bodies can contribute to the onset of dementia within ten years of PD diagnosis due to neuronal death and changes in dopamine levels (Alzheimer's Association, 2022; Davis Phinney Foundation for Parkinson's, 2018). While a correlation is present, researchers are seeking to understand better the greater association between Lewy bodies and PD.
Harvard Stem Cell Institute (2022) is currently examining how modifying skin cells from a patient with PD can induce pluripotent stem cells to differentiate into dopaminergic neurons. UCI Health (2022) is conducting stem cell research on individuals with advanced-stage PD for whom medications are no longer effective. The trial involves surgically implanting differentiated dopamine-producing stem cells into the brain, based on a hypothesis that dopamine-cell replacement therapy may enhance an individual's quality of life and reduce dependence on medication (UCI Health, 2022).
Other Experimental Treatments
In addition to stem cell therapy, neuron-repair treatments, gene therapy, and gene-targeted treatments are being examined for PD (Ntetsika et al., 2021). Neuron-repair treatments are currently being investigated in mice; specifically, re-programming astrocytes has increased new dopaminergic neurons (Wei & Shetty, 2021). Gene therapy and gene-targeted treatments are currently being investigated as disease-modifying and non-disease-modifying options: disease-modifying treatments focus on preventing neuron death or regenerating new neurons, whereas non-disease-modifying therapies focus on symptom management (Axelson & Woldbye, 2018).
MacMahon Copas and colleagues (2021) identified a possible link between inflammation and PD that requires more research. More specifically, the presence of T lymphocytes in patients with PD may signify inflammation. Baird and colleagues (2019) observed T cells in the substantia nigra of PD individuals. Bhatia and colleagues (2021) found that T lymphocyte levels correlated with advanced-stage PD. This research has the potential to impact the direction of the treatment and understanding of PD progression (Baird et al., 2019).
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