Parkinson's Disease: Assessment, Diagnosis, and Management

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


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

In This Article


The main brain structures affected by PD are the substantia nigra pars compacta and the basal ganglia. The basal ganglia controls fine motor movements, and is composed of numerous subcortical nuclei, including the striatum, amygdaloid body, and claustrum. PD symptoms are a result of a loss of dopamine-producing neurons from the substantia nigra pars compacta. The loss of these neurons results in a deficiency of dopamine, a neurotransmitter in the striatum. Dopamine is vital to movement because it promotes the transmission of messages that initiate and control movement and balance. At the time of clinical presentation of PD when motor and balance symptoms occur, up to 70%-80% of the dopamine neurotransmitters may already be lost. Casey[6] proposed that the pathology underlying PD may not be restricted to the substantia nigra or dopamine loss. Gazewood et al[7] suggested that pathologic changes may be detected up to 20 years before the onset of motor symptomatology.

The aging process may be an accentuating or contributing pathophysiologic factor in PD clinical presentation. Dopamine levels decrease as a person ages; therefore, the reduction in dopamine from the aging process and pathophysiologic changes associated with PD may facilitate symptom advancement and support the development of new PD symptoms.

Clinical Presentation

The clinical presentation of PD consists of primary and secondary motor symptoms. In addition, PD clinical presentation may include nonmotor symptoms.

Primary Motor Symptoms

PD is challenging to diagnose in the early stages because the first signs and symptoms are often subtle and vague. There are 4 cardinal symptoms of PD known through the acronym TRAP: Tremor at rest, Rigidity, Akinesia (or bradykinesia), and Postural instability.[8] PD patients often present with diverse lifestyles and profiles; therefore, motor and nonmotor signs and symptoms should be evaluated in the context of each patient's needs and goals.[9]

Resting tremor occurs in the early stages of the disease and is the most common and easily recognized PD symptom. Approximately 70% of PD patients experience a unilateral tremor in the hand or foot.[2] The tremor is described by the patient as "shakiness" or "nervousness" and may have an intermittent presentation. Classically, the tremor is a resting uncontrollable tremor and disappears with the use of the affected limb.[8]

Rigidity is characterized by increased resistance and often described as stiffness in the limbs.[10] Rigidity may be associated with pain. The pain often originates in the shoulder and is commonly misdiagnosed as arthritis, bursitis, or rotator cuff injury.[8]

Bradykinesia, the most characteristic symptom of PD, presents as slowness of movement.[2] Bradykinesia encompasses difficulties with planning, initiating, and executing movement and with performing sequential and simultaneous tasks. Performing repetitive movements, such as finger tapping, and activities of daily living, such as buttoning a shirt, cutting food, or brushing teeth, become difficult.[10]

Postural instability, the imbalance and loss of righting reflexes, is the most common cause of falls contributing to the risk of hip fractures in the PD population. This coordination and balance symptom is generally a manifestation of late-stage PD, which occurs after the onset of other primary motor symptoms.[10]

Secondary Motor Symptoms

In addition to the primary motor or cardinal symptoms, PD patients may exhibit a number of secondary motor symptoms known to impact activities of daily living and quality of life.[10] Dysarthria (motor speech disorder), hypophonia (soft speech), dysphagia (difficulty swallowing), and sialorrhea (drooling or excessive salivation) are frequently observed in PD patients and may be more disabling than the cardinal features. Orofacial-laryngeal bradykinesia and rigidity are thought to cause these symptoms.[8]

Freezing of gait is a secondary motor symptom not explained by bradykinesia or rigidity. With gait freezing, the PD patient will hesitate before stepping forward or experience the inability to continue movements when already in motion. The gait freezing increases the client's fall risk potential.[10]

Micrographia is the shrinkage of handwriting and progresses with increased amounts of writing. Micrographia occurs as a result of bradykinesia.[10]

Mask-like expression, a secondary motor symptom, results from a combination of rigidity and bradykinesia. The PD patient's face will appear less expressive than usual.[10]

Several patients with PD may experience unwanted movement accelerations that also pose a fall risk potential. These are body movements that occur rapidly in an uncoordinated manner. These quick movements are especially troublesome in speech and mobility. Accelerated movement presentation may also cause tachyphemia, also known as cluttering (rapid rate speech that is not understandable).[10]

Nonmotor Symptoms

Nonmotor symptoms are symptoms that do not involve movement, coordination, physical tasks, or mobility. Nonmotor symptoms are an underappreciated aspect of PD clinical presentation. Nonmotor symptoms may precede motor symptoms and a PD diagnosis by several years. Nonmotor symptoms include autonomic dysfunction, cognitive/neurobehavioral disorders, and sensory and sleep abnormalities.[8]

Autonomic dysfunction is common in the PD patient. Features include orthostatic hypotension, sweating dysfunction, sphincter dysfunction, erectile dysfunction (ED), urinary bladder retention, urinary tract infections, and constipation.[10]

Cognitive/neurobehavioral disorders may be as disabling as motor symptoms. Depression, anxiety, apathy, and hallucinations frequently occur in PD patients. PD patients may also present with dementia. As PD progresses, the brain experiences microscopic deposits of alpha-synuclein (Lewy bodies), resulting in memory changes, decreased attention ability, difficulty planning, and problems with decision making. In addition to cognitive and affective disorders, obsessive-compulsive and impulsive behaviors, such as craving, binge eating, pathologic gambling, and compulsive shopping, tend to occur in PD patients. There is also a fascination with repetitive handling, examining, sorting, and arranging of objects.[8] These symptoms are referred to as hedonistic homeostatic dysregulation, which is a neuropsychological behavior disorder associated with the use of dopaminergic drugs, especially a dopamine agonist. Therefore, NPs should monitor the presentation of these nonmotor symptoms when managing the PD patient with a dopamine agonist.

Sleep disturbances, specifically rapid eye movement (REM) behavior disorder, is a substantial risk factor for the development of PD. REM behavior disorder is a preparkinsonian state that occurs in approximately one third of PD patients and is characterized by violent dreams accompanied by hitting or kicking motions, yelling, screaming, and other potentially dangerous motor activity during REM sleep.[10–12]

Fatigue is a common nonspecific complaint. Fatigue can have both mental and physical causes. Muscle stiffness, depression, slow movement, insomnia, and PD medications can also cause fatigue symptoms.[10] PD patients can experience a loss of smell (anosmia). The loss of smell may occur before the onset of other PD signs and symptoms and is a strong predictor of beginning long-term cognitive problems. Table 1 summarizes primary, secondary, and nonmotor PD symptoms.


Differential diagnoses to consider in patients presenting with PD clinical symptoms are essential tremors, vascular parkinsonism, drug-induced parkinsonism, dementia, progressive supranuclear palsy, and multisystem atrorphy.[7] A differential diagnosis of PD is primarily based on a clinical diagnosis. A clinical diagnosis of PD requires the presence of the cardinal signs of distal resting tremor of 3–6 Hz, rigidity, bradykinesia, and asymmetrical onset. In addition, patients diagnosed with PD must respond to an adequate therapeutic levodopa or a dopamine agonist challenge. The clinical diagnosis of PD is further supported by progressive functional and motor impairment. Both computed tomographic (CT) scanning and magnetic resonance imaging (MRI) provide a limited role in the differential diagnosis of PD because they do not show a specific PD pathologic finding. CT or MRI scans are used to facilitate the differential diagnosis of PD and rule out brain tumor or cerebral vascular accident (stroke). The US Food and Drug Administration (FDA) has approved the use of ioflupane iodine-123 injection or DaTscan (GE Healthcare B.V., Eindhoven, The Netherlands) to be used to detect dopamine transporters in suspected PD cases. The DaTscan uses radioactive ioflupane iodine-123 to determine the amount of dopamine available in a person's brain. DaTscan is not used to diagnose PD but rather to assist with confirming a PD diagnosis. Clinical providers who do not diagnose PD frequently are encouraged to refer suspected cases to clinicians who are experienced and frequently diagnose PD as a means of reducing clinical diagnostic errors.[2]