Among the most common neurogenerative diseases, Parkinson’s disease (PD) most often affects people older than age 60. Yet one in 20 patients is younger than 40 when diagnosed. Its cause isn’t known, although research now centers on genetic and environmental factors and brain trauma.
PD is characterized by loss of dopaminergic nerve cells in the substantia nigra of the basal ganglia in the brain’s lower region, on either side of the brainstem. Dopamine is integral to movement coordination; once 70% of dopaminergic nerve cells are lost, PD signs and symptoms become evident. As dopamine levels continue to fall, manifestations become more apparent and new signs and symptoms arise. Another physiologic hallmark of PD is presence of Lewy bodies containing alpha-synuclein in this same brain region.
Cardinal features of PD are bradykinesia, resting tremor, and muscle rigidity. Some patients also have stooped posture, altered gait, dystonia, fatigue, muscle cramps, drooling, sexual dysfunction, masklike facial expression, dysphagia, and speech problems. Signs and symptoms usually are asymmetric and commonly begin with a resting tremor. Over time, they grow progressively worse and more debilitating, and may include cogwheel rigidity and postural instability leading to increased risk of falls. Some patients have “freezing” episodes, which they describe as a feeling that their feet are stuck to the floor. PD also causes autonomic problems, such as genitourinary and GI dysfunction, thermoregulation problems, and orthostatic hypotension. Some patients may complain of sensory symptoms, such as pain, itching, and numbness.
Psychological manifestations may include depression, dementia, memory loss, psychosis, fear, anxiety, and sleep difficulties. Patients may exhibit compulsive behaviors, such as excessive gambling, hypersexuality, excessive eating and shopping, repetitive activities, and medication abuse.
PD can’t be cured. Treatment aims to slow disease progression and reduce disability while minimizing complications. One might think that simply administering dopamine directly into the brain (if that were possible) would cure the disease. But dopamine doesn’t cross the blood-brain barrier, so getting it to its intended target would require more than just dopamine administration. Also, many medications have adverse effects, and multiple drugs are needed to treat all aspects of the disease. (See chart by clicking the PDF icon above.)
Levodopa and carbidopa
Treatment focuses on symptom management, and levodopa (L-dopa) remains the gold standard. The immediate precursor of dopamine, L-dopa is converted to dopamine by decarboxylation both in the brain and peripheral tissues. L-dopa is given in combination with carbidopa to minimize peripheral conversion, which allows more of the drug to reach the brain and thus prevent nausea. A peripheral decarboxylase inhibitor, carbidopa replaces the dopamine lost in PD. It takes effect within 15 to 30 minutes of administration. Levodopa is combined with carbidopa in various medications, including Sinemet, Sinemet CR, and Parcopa (orally disintegrating tablets). Stalevo combines L-dopa, carbidopa, and entacapone, a catechol-O-methyltransferase (COMT) inhibitor designed to inhibit end-of-dose “wearing off.” Unfortunately, clinical benefits of these drugs decline over time, necessitating additional doses, which in turn may cause dyskinesia.
Dopamine agonists stimulate dopamine receptors, allowing the brain to recognize it’s receiving dopamine. These drugs help decrease end-of-dose wearing off, “on-off” motor fluctuations (such as “freezing”), and dyskinesia.
Dopamine agonists also have neuroprotective effects. When given as adjuncts to levodopa, they may permit downward titration of the levodopa dosage. However, they’re more likely to cause neuropsychiatric adverse effects, such as hallucinations, psychosis, and compulsive behaviors. Dopamine agonists available in the United States include bromocriptine (Parlodel), pramipexole (Mirapex), ropinirole (Requip), and apomorphine (Apokyn injection). Possible adverse effects include nausea, vomiting, back pain, and nightmares.
Amantadine (Symmetrel) is an antiviral dopamine agonist used as a secondary drug for patients with muscle rigidity and tremors. In combination with levodopa-carbidopa, it can extend the patient’s “on time” (the duration for which the drug is effective). Apomorphine is a subcutaneously injected dopamine agonist used as a rescue drug for immobility episodes; a prominent adverse effect is vomiting, which warrants addition of trimethobenzamide (Tigan), an antiemetic.
Used as adjuncts to levodopa-carbidopa, COMT inhibitors block some peripheral breakdown of levodopa, allowing more levodopa to reach the brain. As a result, they help improve motor fluctuations and reduce end-of-dose wearing off. Two COMT inhibitors used in the United States are tolcapone (Tasmar) and entacapone (Comtan). Entacapone may cause dyskinesia, GI upset, dizziness, and drowsiness. Tolcapone may cause similar adverse effects, plus excessive dreaming, increased sweating, and hepatotoxicity.
Monoamine oxidase type-B inhibitors
Monoamine oxidase type-B inhibitors (MAOBIs) may be used to treat PD in early or late disease stages. The enzyme MAOB aids dopamine breakdown in the brain. In the early PD stages, MAOBIs can help delay the need for levodopa-carbidopa. In late disease stages, they may be used as adjuncts to levodopa-carbidopa to prevent its breakdown, thus helping more drug reach the brain. Available MAOBIs in this country are selegiline (Eldepryl, Carbex), the selegiline orally disintegrating tablet (Zelapar), and rasagiline (Azilect). Rasagiline may decrease freezing episodes as levodopa effects wear off. Adverse effects of MAOBIs include increased systolic pressure, arthralgia, depression, delirium, and hypotension.
Transdermal and duodenal drug administration
Some medications may be delivered transdermally or by enteral duodenal infusion. A transdermal patch delivers a dopamine agonist around the clock to decrease “off time”; it’s used in combination with L-dopa. Duodenal infusion avoids gastric emptying problems. It can be used short-term through a nasogastric tube and long-term through a percutaneous endoscopic gastrostomy tube that extends into the duodenum. These methods are still under review.
Managing psychological effects
Clinicians should address the psychological needs of patients with PD and their family members or other caregivers. Psychological effects may include distress, decreased quality of life, and other sequelae of poor PD outcome. Many PD patients suffer from depression and are treated with antidepressants—most commonly selective serotonin reuptake inhibitors (SSRIs), such as fluoxetine, escitalopram, sertraline, paroxetine, and citalopram.
Other antidepressants that may be used adjunctively include venlafaxine, mirtazapine, bupropion, and nortriptyline. Nortriptyline must be used cautiously in elderly patients due to the risk of increased orthostatic hypotension, cognitive impairment, and constipation.
Changes in the noradrenergic system and chemical imbalances of dopamine, serotonin, gamma-aminobutyric acid, and glutamate can lead to anxiety. Some PD patients exhibit panic disorder, agoraphobia, and obsessive-compulsive disorder. Anxiety sometimes is linked to motor control problems related to levodopa levels. To treat anxiety, the physician may prescribe SSRIs, venlafaxine, mirtazapine, or bupropion. Such drugs as lorazepam, alprazolam, and clonazepam may be used to treat acute anxiety attacks.
Some patients may be candidates for deep brain stimulation. (See the box below.) Complementary and alternative modalities may be used as well, including massage therapy, reflexology, Reiki, and various herbal medicines. Results of these treatments vary, and the effectiveness of some is still being studied.
Physical therapy, occupational therapy, and speech and language therapy may be helpful. Physical therapy can increase the ability of PD patients to move. A physical therapist works with the patient on safe and effective ways of sitting, standing, and walking, and assesses the need for ambulatory devices as PD progresses. An occupational therapist can help patients cope with the effects of PD on daily routine and activities of daily living, and help them with adaptations to skills requiring fine motor coordination.
Speech and language therapists can help patients strengthen the volume of their voices so they can continue to participate in conversation and feel comfortable in social situations. Also, they can assess and improve swallowing difficulties (common in PD patients).
Deep brain stimulation
Although drugs are a vital component of PD treatment, other treatments exist. In deep brain stimulation (DBS), an electrode is implanted in the patient’s brain through a small opening in the skull. The electrode has an extended insulated wire that’s passed under the skin of the head, advanced through the neck and shoulder, then attached to a neurotransmitter or battery pack placed under the collarbone or lower in the chest (similar to a pacemaker). The device delivers electrical stimulation to the brain areas that control movement, blocking the abnormal signals that cause tremors and easing slowness of movement and stiffness. In addition, DBS may allow patients to receive lower medication dosages.
Not all patients are DBS candidates. Eligibility criteria include:
The patient’s cognitive function is an important consideration. Generally, patients who frequently become disoriented and have significant memory or cognitive problems aren’t ideal DBS candidates. Patients undergoing DBS need cognition adequate for them to participate in an “awake&34; surgery and tolerate many programming visits and medication adjustments.
Contraindications to DBS include:
Postoperatively, assess for typical postsurgical complications, such as signs and symptoms of infection. Teach the patient and family about the need for follow-up visits to adjust neurotransmitter settings and manage changes in PD signs and symptoms as the disease progresses.
Nursing responsibilities for patients with PD include drug administration and patient and family education. Make sure you’re familiar with the mechanisms of action of PD drugs, importance of taking drugs exactly as scheduled, and drug contraindications and adverse effects. For patients on L-dopa, explain that they shouldn’t take this drug with high-protein meals as this can reduce its absorption and availability. Caution them to avoid foods and supplements high in pyridoxine (vitamin B6), which can inhibit the drug’s action. Although L-dopa can be taken with food to relieve GI adverse effects, it may compete for absorption with amino acids in foods. Advise the patient to gradually move back the dosing time to 30 minutes before meals to decrease GI problems and reduce competition with amino acids. Tell patients and family that taking L-dopa on an empty stomach increases its absorption.
Teach patients and caregivers about other adverse drug effects and how to deal with them. Stress the importance of taking drugs on time, and review possible consequences of taking them late or missing a dose. Also provide education on PD progression and explain that as the disease progresses, changes in medication dosing and frequency may be required.
Discuss the importance of exercise. For instance, many patients enjoy dancing, which provides both a psychological lift and a physiologic benefit. Exercise has been found to:
- improve neuromuscular interaction and neurogenesis
- help initiate functional and morphologic changes in the brain
- help slow PD progression
- increase serum calcium levels, thus raising dopamine concentration (higher calcium levels help mediate stress resistance)
- hinder inflammation by activating anti-inflammatory molecules that slow degeneration of dopamine-containing neuronal cells.
PD has many facets. As a nurse, you need to be able to recognize and address all aspects of the disease and understand the importance of changing medications and therapies as the disease progresses. To help the patient and family cope with PD, direct them to available resources, such as support groups and PD organizations.
Ahmed BY. Exercise as a neuroprotective mechanism in Parkinson’s disease: future treatment potential? Brit J Neurosci Nurs. 2008 Nov 14;4(11):525-30.
Bostwick JM, Hecksel KA, Stevens SR, Bower JH, Ashlskog JE. Frequency of new-onset pathologic compulsive gambling or hypersexuality after drug treatment of idiopathic Parkinson disease. Mayo Clin Proc. 2009;84(4):310-6.
Bunting-Perry LK, Vernon GM. Comprehensive Nursing Care for Parkinson’s Disease. New York, NY: Springer; 2007.
Cranwell-Bruce LA. Drugs for Parkinson’s disease. Medsurg Nurs. 2010 Nov-Dec;19(6):347-9.
Heisters D. Parkinson’s: symptoms, treatments and research. Br J Nurs. 2011 May 13-26;20(9):548-4.
Hermanns M. Parkinson’s focus. Parkinson’s is debilitating but new treatments are on the horizon. RN. 2008 Oct;71(10);24-8.
Lindahl DA. Parkinson’s: treating the symptoms. Br J Nurs. 2011 Jul 28-Aug 4;20(14):852-7.
Lo K, Leung K, Shek A. Management of Parkinson’s disease: current treatments, recent advances and future development. Formulary. 2007 Sep;42(9):529-44.
National Institute of Neurological Disorders and Stroke. NINDS deep brain stimulation for Parkinson’s disease information Page. (Updated February 7, 2012.) www.ninds.nih.gov/disorders/deep_brain_stimulation/deep_brain_stimulation.htm#What_is. Accessed August 8, 2012.
Okum MS, Fernandez HH, Rodriguez RL, Foote KD. Identifying candidates for deep brain stimulation in Parkinson’s disease: the role of the primary care physician. Geriatrics. 2007 May:62(5):18-24.
Sydow O. Parkinson’s disease: recent development in therapies for advanced disease with a focus on deep brain stimulation (DBS) and duodenal levodopa infusion. FEBS J. 2008 Apr;275(7);1370-6.