Parkinson's Disease: Assessment, Diagnosis, and Management

Leslie F. Nolden, DNP, FNP-BC; Todd Tartavoulle, DNS, CNS-BC; Demetrius J. Porche, DNS, PhD

Disclosures

Journal for Nurse Practitioners. 2014;10(7):500-506. 

In This Article

Clinical Management

Clinical management involves motor symptom treatment, which does improve functional ability. Clinical symptomatic management may impact PD prognosis. Clinical management consists of early and late medical management. PD patients should be followed up at least every 6–12 months; however, follow-up care depends on clinical symptom progression and response to pharmacologic management.

Early Medical Management

Once patients with PD develop functional disability, the American Academy of Neurology recommends initiating early medical management. General guidelines for treatment regimens exist; however, each client must have an individual evaluation to determine the most effective initial pharmacologic agent or combination of agents that is most likely to impact the loss of dopamine in the brain and the initial presenting clinical symptoms. Levodopa, nonergot dopamine agonists, and monoamine oxidase B (MAO-B) inhibitors can be used for initial therapy.[7] Table 2 summarizes the FDA–approved medications for PD.

Levodopa, administered with carbidopa, remains the primary treatment for symptomatic patients. Carbidopa inhibits peripheral metabolism of levodopa, thereby increasing levels of cerebral levodopa to a therapeutic concentration.[7] The combination of levodopa/carbidopa (Sinemet; Bristol-Myers Squibb Pharma Company, New York, NY) is the most effective agent available to treat PD motor symptoms. The early use of levodopa/carbidopa may result in dyskinesias.[7]

Nonergot dopamine agonists pramipexole (Mirapex; Boehringer Ingelheim Pharmaceuticals, Inc., Ridgefield, CT) and ropinirole (Requip; GlaxoSmithKline, Middlesex, UK) directly stimulate dopamine receptors in the brain and are used alone or in combination with levodopa/carbidopa to treat PD motor symptoms. These 2 pharmacologic agents are not as effective as levodopa in treating motor symptoms; however, the nonergot dopamine agonists do have a lower incidence of dyskinesias.[7]

Ergot-derived dopamine agonists cabergoline bromocriptine (Parlodel; Validus Pharmaceuticals LLC, Parsippany, NJ) and pergolide (Permax; Eli Lilly and Company, Boston, MA) should not be used as a first-line treatment because of the risk of serosal fibrosis and cardiac valvulopathies.[7] If used, baseline and annual transthoracic echocardiograms, chest x-ray, and testing of erythrocyte sedimentation rate and renal function are required.[7]

MAO-B inhibitors block the action of the MAO enzyme that breaks down dopamine and may be used in early medical management. Fewer incidences of dyskinesia and adverse effects occur with MAO-B inhibitors compared with levodopa/carbidopa. MAO-B inhibitors are less effective in treating motor symptoms than dopamine agonist.[7]

Late Medical Management

As PD progresses, additional motor complications, such as dyskinesias and motor fluctuations, develop, and initial medical management becomes no longer as effective. "On time" refers to the time when medication is effectively controlling the disease's symptoms, and "off time" occurs when disease symptoms recur gradually or abruptly. As PD progresses, on time becomes shorter, causing complications that can impair quality of life.[7]

Dopamine agonists, nonergot dopamine agonists, MAO-B inhibitors, and catechol O-methyltransferase (COMT) inhibitors may be used as adjunctive therapy to decrease off time. COMT inhibitors tolocapone (Tasmar; Valeant Pharmaceuticals International, Inc., Steinbach, MB, Canada) and entacapone (Comtan; Novartis Pharmaceuticals Corporation, East Hanover, NJ) are administered with levodopa and prolong symptom relief. The COMT inhibitor tolcapone (Tasmar) is rarely prescribed because it is associated with fatal hepatotoxicity.[7] A Cochrane review concluded that dopamine agonists were most effective with reducing off time.[13]

Surgery

Despite optimal medical management, most PD patients will develop disabling symptoms that may make them a candidate for deep brain stimulation (DBS). Candidacy for DBS is a careful and considerate process. The PD patient must be screened for depression and suicidal ideation before DBS therapy is considered an option. DBS assists with dyskinesia and gait freezing.

DBS targets either the subthalamic nucleus or the globus pallidus interna to effectively improve motor function and reduces motor fluctuations and dyskinesias. DBS may or may not decrease antiparkinson medication use (may or may not increase on time). DBS relief of motor symptoms may improve quality of life. DBS does not slow pathologic progression but impacts clinical symptom presentation.[7]

Alternative Therapy Management

Alternative therapies may provide symptomatic relief to the PD patient. Acupuncture is widely used and may have symptomatic benefits for motor and nonmotor symptoms.[14] Manual therapy and exercise interventions (aerobic exercise), including chiropractic manipulation, osteopathic manipulation, and Trager therapy, may benefit patients with PD; however, no research findings refute or confirm this position.[14] Trager therapy is a type of massage that involves rhythmic touch and movement exercises. The goal of Trager therapy is to generate positive feelings, connect mind and body, promote relaxation, improve mobility, and clear the mind. Trager therapy is used in PD patients to reduce muscle rigidity.

Quality of Life and Caregiver Issues

Nonmotor symptom fatigue may occur early during PD presentation. As PD progresses, nonmotor symptoms significantly decrease quality of life. Early recognition and treatment of these symptoms will improve quality of life for both patients with PD and their caregivers. Table 3 presents a list of resources to assist both the PD patient and primary caregiver.

Orthostatic hypotension, ED, urinary incontinence, and constipation may appear late in PD progression. These symptoms negatively impact the PD patient's quality of life. The PD patient must exercise caution to reduce the incidence of falls that further reduce their ability to remain physically active and socially engaged. This fall risk increases the need for the primary caregiver to remain aware of the environmental conditions that may increase the PD patient's fall potential. Interventions to impact the fall risk potential include activities such as using ambulation aids like laser canes or walkers, eliminating moveable rugs from the client's environment, reducing glare and clutter in the home, using nonskid surfaces, placing handrails along stairs/steps and in the bathroom, raising the toilet seat level, and lowering the bed level.

Freezing during movement is associated with increasing the PD client's fall risk. Interventions to impact fall risk associated with freezing includes weight shifting from 1 leg to the next while in motion, listening to music and stepping with the rhythm, focusing on a floor target to step on, and imagining a line on the floor to step on while walking.

ED also impacts both PD patients' and their significant others' sexual health. Clients experiencing ED can be treated with different modalities, such as cognitive/behavioral and pharmacologic interventions. ED management consists of sexual counseling, vacuum pump devices, penile implantation, and pharmacologic management, such as sildenafil and apomorphine.

Depression is another symptom that compounds the impact of PD symptoms on the patient's quality of life. The Beck Depression Inventory may be used as a screening tool for patients in whom depression is suspected. The common treatments for depression, cognitive behavioral therapy and pharmacologic therapy, should also be implemented in the PD patient. Pharmacologic therapies include the selective serotonin reuptake inhibitors citalopram (Celexa; Forest Pharmaceuticals, Inc., St. Louis, MO), sertraline (Zoloft; Pfizer, New York, NY), and fluoxetine (Prozac; Eli Lilly and Company) and the serotonin and norepinephrine reuptake inhibitors venlafaxine (Effexor; Pfizer) and duloxetine (Cymbalta; Eli Lilly and Company). The tricyclic antidepressants should be used with caution in treating depression in PD patients. Tricyclic antidepressants can cause anticholinergic adverse effects and exacerbate orthostatic hypotension.[15]

The ability to communicate may negatively impact quality of life. Speech therapy is frequently used to treat the development of dysarthria. Individual speech therapy aimed at phonatory efforts may improve speech volume and improve the client's ability to communicate.

The Lee Silverman Voice Treatment (LSVT) is to increase vocal intensity in PD patients. LSVT focuses on a set of voice exercises that are practiced intensively, 4 sessions per week during a 4-week period. The goal of LSVT is to improve vocal performance by maximizing vocal effort ("think loud, think shout") and sensory perception of vocal effort. LSVT has resulted in normal speech and voice quality in some patients.

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