Nicole Ramos

Dr. Krasilovsky
Differential Diagnosis & Intervention in Clinical Neurology
Case History Parkinsons Disease

Overview of the Disorder

Parkinsons Disease is a degenerative movement disorder affecting the central nervous

system and its ability to maintain normal motor function. It is marked by resting tremors,

rigidity, bradykinesia, and a shuffling gait (Mayo Clinic Staff, 2015). Approximately 1 million

people in the United States are living with Parkinsons, and 1 out of every 3 adults over the age

of 85 years will have the disease (Umphred, 2012). Parkinsons disease also holds a greater risk

for males, as they are 1.5 times more likely to contract the disorder than females (www.pdf.org).

The etiology is precisely unknown, but largely thought to arise from a combination of genetic

factors and undetermined environmental triggers (Huang, Z., de la Fuente-Fernndez, R., &

Stoessl, A. J., 2003). However, the scientific community has not yet reached a consensus on

which factor plays the dominant role. Environmental risk factors include exposure to pesticides

or metals, as well as rural living and drinking well-water (Huang, Z., et. al., 2003). Some of the

genetic risk factors that have been identified include 6 different genes that studies have shown to

cause familial Parkinsons disease (Schapira, A. H., 2006). Some studies show that smoking

cigarettes, coffee and caffeine consumption, the use of NSAIDs all play a role in lowering the

risk of developing Parkinsons. Others point to head trauma, dietary consumption of lipids and

dairy, or high caloric diets as factors that increase risk (Chade, Kasten, & Tanner, 2006). And so,

the fact remains that Parkinsons disease is an idiopathic disorder.

Parkinsonism is an umbrella term that is used to refer to a number of basal ganglia

disorders that result in bradykinesia, resting tremors, and stiffness. Classic idiopathic Parkinsons
disease is the most common cause of parkinsonism. Atypical Parkinsons disease or Parkinson-

plus syndromes affect 10% of the cases diagnosed as parkinsonism. Additionally, it can be

difficult to distinguish in early stages from classic Parkinsons disease.

Parkinsons disease is progressive. However, the speed of this progression will vary

depending on age, stage of the disease, and patient history of pharmacological treatment. For

example, motor symptoms of Parkinsons can advance rapidly if left untreated. However, one of

the very common medications (Levodopa) used to address those motor symptoms carries long

term risks of its own, such as toxicity, diskynesia, and motor fluctuations.

Pathology

Parkinsons Disease is a disorder affecting the basal ganglia of the central nervous

system. The basal ganglia are made up of the globus pallidus and the neostriatum (which is itself

composed of the caudate and the putamen). These three separate nuclei are located near the base

of the cerebral cortex. The substantia nigra, subthalamic nucleus, and 2 brainstem nuclei are also

considered part of the basal ganglia due to their functional connection with the forebrain nuclei.

(Umphred, 2012). The basal ganglia functions as part of the extrapyramidal system that plays a

role in all motor control, along with the pyramidal system and the cerebellum. The basal ganglia

receive input from the substantia nigra p.c. and the motor cortex, it then sends signals back to

these locations via two pathwaysthe direct and indirect pathways. Current theories also

suggest that the basal ganglia play a role in action selection. Action selection is the process of

choosing one of several possible actions or behaviors to perform at any particular time

(Humphries, Stewart, & Gurney, 2006). Patients with Parkinsons often experience difficulty

with movement initiation. The role the basal ganglia play in movement selection could

potentially explain this phenomenon.

 Much of the dopamine neurons that exist in the midbrain originate in the substantia nigra

p.c. The dopamine is responsible for the dark color that gives the substantia nigra its name. The

substantia nigra p.c. projects its dopamine neurons to the neostriatum, creating a pathway that is

very important in facilitating movement. The neostriatum receives input from two sources

onlythe cortex and the substantia nigra p.c. The input received the from the cortex is excitatory

via the neurotransmitter GABA. The input received from the substantia nigra p.c. provides post-

synaptic inhibition via the neurotransmitter dopamine. It is this projection that is implicated in

Parkinsons disease and parkinsonism.

Parkinsons disease is marked by the gradual loss of dopamine-releasing neurons in the

substantia nigra p.c. Normally, the substantia nigra p.c. releases dopamine to the striatum that

activate the direct pathway of the basal ganglia via D1 receptors, and inhibit the indirect pathway

via D2 receptors. Often, by the time Parkinsons motor symptoms present themselves, 60-80% of

these cells are already lost. As indicated earlier, the precise cause of this cell death remains

unknown. Nevertheless, once these cells perish, decreased quantities of dopamine to the striatum

results in unchecked output from the globus pallidus internus and substantia nigra pars reticulata

to thalamus. This, in turn, reduces excitation of the motor cortex and thus, suppresses movement.

(Galvan & Wichmann, 2008).

Clinical Manifestations & Differential Diagnosis

The three cardinal signs of Parkinsons disease are bradykinesia, rigidity, and resting

tremors. While there are non motor symptoms, they generally present once the disease has

progressed and motor deficits have already materialized. Therefor, we will focus on the motor

clinical manifestations.
 Bradykinesia is a negative sign. In other words, functions normally seen in a healthy

individual would be diminished or absent in an individual Parkinsons disease. Bradykinesia,

described often as a decrease or poverty of motion, is marked by the individuals inability to

initiate or perform purposeful movement. It is pervasive for all types of movement, but complex

movement patterns are affected more than simpler ones. Umphred uses the example of executing

dorsiflexion during gait at toe-off vs performing dorsiflexion while seated in a chair (2012). A

patient with Parkinsons would exhibit more difficulty with the former. In addition to the

execution of movement, patients have difficulty with the initiation of movement. When

manifested as a complete absence of movement initiation, it is referred to as akinesia. A classic

example of lack of initiation is the sign mask face; the Parkinsons patient is unable to laugh at

a joke because they are unable to implement a facial response. Umphred also places transitional

difficulties under the umbrella of bradykinesia. These patients often exhibit difficulty performing

sequential or simultaneous tasks; needing to complete one motor task before beginning the next,

as well as exhibiting a noticeable lack of planning (Umphred, 2012). This becomes most

noticeable if the sequential tasks are constantly changing vs repetitive. A Parkinsons patient

would also show noticeable difficult in motor tasks requiring multiple movement patterns,

agility, and/or change of direction and exhibit an easier time operating an upper body ergometer.

This has clinical implications for physical therapy management that will be discussed later in

more depth.

Rigidity is defined as an increased resistance to passive movement. It is not to be

confused with spasticity, which is a velocity dependent increased response to stretch. Cogwheel

rigidity is the kind most commonly associated with Parkinsons. It is a positive sign,

characterized by an increased resistance to passive movement throughout the entire range,

regardless of direction. A positive sign is one that normally absent in a healthy individual, but

present in the affected patient. Unlike spasticity, it is not an increase in gamma motor neuron

response. Cogwheel rigidity occurs due to an increase in motor drive from anterior horn cells. It

is important to note that rigidity may result in greater energy expenditure (Umphred, 2012). This

has clinical implications for patient perceptions of fatigue and effort, as well as movement or

exercise difficulty.

The cardinal, positive sign of tremors is of note because they specifically occur only at

rest. Seventy percent of individuals with Parkinsons disease in early stages will experience an

asymmetrical tremor in the distal upper or lower extremity (pdf.org). Active and purposeful

movement will cause the tremor to either decrease or disappear completely. Parkinsonian resting

tremors generally have a frequency of 4 to 7 Hz. The tremors are usually seen distally, such as in

the hand, however some Parkinsons patients present with a postural tremor. Resting tremors in

the hands is classically described as pill rolling of the thumbs and figures. And although

resting tremors initially present asymmetrically, they will eventually move to a symmetrical

presentation as the disease progresses. It is worth noting, however, that although it presents an

aesthetic disability, resting tremors do not generally present a huge problem functionally. Most

of the time, resting tremors do not interfere with activities of daily life since they decrease or

vanish with purposeful movement (Umphred, 2012). Interestingly enough, while one of the most

notorious early signs of Parkinsons, it also does not need to be present for an individual to

receive a Parkinsons disease diagnosis.

Postural Instability is an extremely important sign of Parkinsons disease. Fifty percent of

individuals with Parkinsons report falling at least once per year. According to Umphred, these

individuals are nine times more likely to have recurrent falls compared with age-matched control
subjects (2012). Postural instability includes difficulty in equilibrium righting reactions.

Protective instincts such as the outstretched arm during falling are noticeably diminished in these

patients. This makes the increased falls risk associated with Parkinsons disease all the more

treacherous.

Festinating gait is the final clinical presentation we will discuss in detail. The name is

derived from the Latin verb for to hurry. This altered gait pattern is a hallmark of Parkinsons

disease. It is marked by a decreased stride length that appears similar to shuffling, accompanied

by decreased velocity of movement. Generally, there is also a notable lack of swing through the

upper extremity that is said to be linked to decreased initiation. An individual with Parkinsons

would have trouble both initiating and ceasing movement, the latter being another clinical

manifestation of Parkinsons disease.

Parkinsons disease is clinically distinct from parkinsonism and Parkinsons plus

Syndromes, though the three do have overlap of certain symptoms. Parkinsons plus syndromes

is a term used to describe several other neurodegenerative illnesses. Parkinson plus syndromes

each have their own unique list of symptoms that are used to diagnose. Unlike Parkinsons

disease, these illnesses do not usually respond to the medication Levodopa, a drug that increases

brain levels of dopamine and has become one of the standard medications in treating Parkinsons

disease. We will explore this more in a later section. Parkinsonism, as mentioned earlier, refers

to diseases whose common link is an insufficiency of dopamine within the basal ganglia. In order

to diagnose parkinsonism, an individual must present with at least two of the following

symptoms: tremor, bradykinesia, postural instability, and rigidity. One of the two symptoms

must be either tremor or bradykinesia. (pdf.org). When trying to distinguish between Parkinsons

disease and Parkinsons plus syndromes, there are some differences in the initial signs that
clinicians can look for. Firstly, tremors, which are a common initial sign in Parkinsons disease,

are generally not present for Parkinsons plus. Initial signs generally not present in Parkinsons

disease that are often seen for Parkinsons plus include: early and/or severe dementia and

difficulty with voluntary eye movements.

General Medical Management

There is currently no cure for Parkinsons disease. The goal of medical management is to

control and mitigate the signs and symptoms of Parkinsons disease while also respecting

potential adverse effects that result from medical treatment. Pharmacological management is

focused by the knowledge that Parkinsons symptoms arise from the decrease in dopaminergic

neurons (Umphred, 2012).

Levodopa has been in use for treating Parkinsons disease since the late 1960s. It

functions by increasing dopamine levels via the dopamine chemical precursor L-DOPA; which,

unlike dopamine, has the ability to cross the blood-brain barrier. It is absorbed from the small

intestine into the blood stream. Once in the brain, the body converts L-DOPA to dopamine.

Levodopa is used to address tremors, poor motor control, stiffness, bradykinesia, and spasms

associated with Parkinsons disease.

Like many drugs, levodopa has side effects. Nausea and vomiting often occur when

taking levodopa, and so it is often combined with carbidopa. Carbidopa serves two functions; it

reduces nausea caused by levodopa, and enhance the dosage effectivity of levodopa. Carbidopa-

levodopa enables the L-DOPA dose to be reduces by as much as 80% (www.parkinson.org).

This combination drug has become a cornerstone in the medical management of Parkinsons

disease, as it provides the greatest therapeutic benefit.

 It is important to note that a side effect associated with long-term use of levodopa is

dyskinesia (Marsden, 1994). Dyskinesia is a movement disorder characterized by abnormal

involuntary muscle movements that Parkinsons patient may not even be aware of. It can be

described as a wiggly or rounded movement, similar to a smooth tic. For some patients, the

dyskinesia associated with levodopa drug use is comparably as disabling as the Parkinsons

symptoms themselves (Michael J. Fox Foundation, 2012). Other patients feel the tradeoff is

warranted if the drug will reduce the stiffness, tremors, and bradykinesia they experience as part

of their disease (Veterans Health Admin, 2015). Dyskinesia is usually heightened at the peak of

dopamine absorption. Therefore, patients can discuss with their physician the best way to

manage their medication schedule or dosage to mitigate these effects.

Dopamine agonists are also employed in the medical management of Parkinsons disease.

They function to stimulate the dopamine receptor pathways even in the absence of sufficient

dopamine in the body. They can be used in isolation to treat the disease in its early stages, or in

combination with levodopa particularly with patients who are experiencing a deteriorating

response to levodopa. A potential side effect of high doses of dopamine agonist medication is

impulsive behavior. This includes kleptomania, trichotillomania, and hypersexuality. These side

effects usually diminish within a week of lowering the dose. (Veterans Health Admin, 2013).

Other medications that are employed include anticholinergics and MAO-B inhibitors.

Anticholinergics restore balance by reducing the effects of overactive acetylcholine, and are

effective in reducing resting tremors. MAO-B inhibitors disrupt the enzyme that breaks down of

dopamine in the brain. This increases the bio-availability of dopamine, thus mitigating some of

the motor symptoms of Parkinsons disease. Like anticholinergics, it can be used as a

monotherapy or in tandem with other medications. ("Parkinson Disease Medication", 2017).

 Deep brain stimulation is a surgical procedure that is often used to address dyskinesia,

other Parkinsons symptoms, and also has therapeutic benefits for non-Parkinson disorders as

well. A neuro-stimulator, often referred to as a brain pacemaker, is implanted as electrodes in

the brain through which electrical impulses will be sent to specific nuclei targets. The two most

commonly targeted site are the subthalamic nucleus and the globus pallidus internus (Plaha,

2006). Deep brain stimulation is thought to inhibit overactive acetylcholine pathways between

the globus pallidus internus, thalamus, or subthalamic nucleus.

Implications for PT (general sense)

Pharmacological therapies are vital in mitigating signs and symptoms of Parkinsons

disease. However, as each patient living with Parkinsons experiences the disease in a

completely unique way, drug therapy alone can never fully address the particular impairments

and dysfunctions faced by each individual. Including physical therapy as a part of the plan of

care for a Parkinsons patient is thus extremely important. Parkinsons disease is, after all,

considered a movement disorder.

Research shows that exercise is invaluable in helping Parkinsons patients maintain

quality of life. decrease stiffness, improve balance and coordination, manage dual tasks: such as

opening a bottle while maintaining gait (Goodwin, Richards, Taylor, Taylor, & Campbell, 2008).

The National Parkinson Foundation (NPF) promotes exercise as essential in soliciting good

outcomes in Parkinsons patients. They highlight that exercise can help with both management of

symptoms and potentially slowing disease progression. NPF also cites a Parkinsons Outcomes

Project study that has shown that participants with Parkinsons who exercised vigourously for

2.5 hours per week showed a decrease in the rate of decline in quality of life

(www.parkinson.org). Neurologists within the NPF network all recommend intense weekly
exercise to their patients. Studies have shown that aerobic exercise induces neuroplastic effects

the circuitry and synapse level, and can even create improved and more efficient uptake of

available dopamine at the receptor sites.

Since Parkinsons disease is a progressive disorder, it is important that patients seek out a

physical therapist immediately following diagnosis. Even if the symptoms are not yet incredibly

involved, a physical therapist can help to establish a baseline of the patients physical ability and

create an appropriate exercise program and schedule specific to the patient. As the disease

progresses, the physical therapist may be the first to notice nuanced changes in the patients

physical ability, functional impairments, or symptom advancement. As the patient becomes more

involved, the physical therapist can help the patient develop energy and motor efficient strategies

for managing ADLs such as getting in and out bed, performing dual tasks safely, retaining status

as a community ambulatory, and maintaining functional strength.

Parkinsons patients often experience symptoms on one side of the body more than

another. This can lead to patient neglect of the more involved side and overuse of the lesser

involved side. Physical therapy can work to retain balance by forcing the patient to exercise and

perform tasks using the more involved side. This can help to improve function and increase

patient awareness. The effectiveness of this has been shown both with Parkinsons and stroke

patients ("Parkinson's Disease Clinic and Research Center", 2012).

As previously mentioned, research shows that at least half of Parkinsons patients report

falling a minimum of once per year. Physical therapy can help address this. Postural instability

causes difficulty with balance, weight shifting, and agility. Physical therapy has been shown to

significantly improve outcome of balance tests in Parkinsons patients including tasks such as

tandem stance, single limb stance, and external perturbation (Stankovic, 2004).
Case Scenario & Recommended PT Program

Case Scenario
Patient is a 63 y.o. female, capable of ambulating. C/o decreased balance, fatigue,

morning stiffness, dyskinesia, and lack of interest in engaging in social activities for the past 2

years. Patient has no history of infection or illness in the past 5 years. Patient was diagnosed with

Diabetes mellitus 8 years ago. She manages her DM with diet only, no medication. Patient was

diagnosed with idiopathic Parkinsons disease 3 years ago. Symptoms began with a tremor in her

right hand, noticed by her husband. Onset of drug related dyskinesia 8 months ago. Patient takes

Levodopa-Carbidoba. Subject is a 1st grade school teacher and works at a school 1 mile from her

home. She lives on the 5th floor of an elevator building with no steps to enter. However, patient

must manage 2 flights of stairs, totaling 24 steps every day at work. Patient expressed an interest

in continuing to work for as long as she can. Patient is currently independent in all activities. She

chose to install hand rails and a shower chair in her bathroom because she is afraid of falling in

the shower. Patients claims no history of falls. Patient is left-handed. Resting tremors noted

during subjective examination.

Objective motor examination revealed good muscle efficiency in all 4 extremities;

however deep tendon reflexes were diminished. MMT examination revealed grade of 4- in all

extremities. There was a mild non-velocity dependent resistance to stretch that would be a grade

1 on the Modified Ashworth Scale (slight increase in muscle tone, manifested by a catch and

release, followed by min resistance throughout the remaining ROM). All sensory functions

(peripheral and cortical) were normal. The patient presented with an independent gait; the gait

pattern showed early signs of festination, and postural assessment revealed slight forward head,

slight forward trunk lean and rounded shoulders. Movements exhibited signs of bradykinesia.
Reciprocal arm swing while walking was diminished. Patient has a FIM score of 7fully

independent in all activities. Based on the assessment, the patient can be classified on the Hoehn

and Yahr scale as a Stage 2Bilateral Involvement.

Practice Pattern 5E: Impaired Motor and Sensory Integrity Associated with Progressive
Disorders of the CNS

Impairments

Decreased balance
Bradykinesia
Fatigue
Stiffness
Dyskinesia
Decreased Muscle Strength
Mild rigidity

Functional Limitations

Altered Gait Pattern- Festinating

Decreased coordination
Decreased motor control
Decreased ability to transition between tasks

Patient Goals

Get stronger
Be able to lift and hold grandchildren
Have enough stamina to keep working as 1st grade teacher

Physical Therapy Long Term Goals: 8 weeks

Improve balance by 25-30%, as measured with Berg Balance Scale and MiniBESTtest
against baseline score
Improve strength to MMT Grade 4+ or 5, as dictated by improvement achieved at week 4
Improve gait mechanics
Improve patient proprioception
Eliminate forward head & shoulder posture, as measured against postural assessment grid
Physical Therapy Short Term Goals: 4 weeks

Improve balance by 12-15%, as measured with Berg Balance Scale and MiniBESTtest
against baseline score
Improve strength to MMT Grade 4 or 4+
Improve coordination
Improve agility
Reduce forward head and shoulder posture, as measured against postural assessment grid

Physical Therapy Exercise Program

Program 1: ***Only move to progressions once proficient in the initial movement. Master
Progression 1 before attempting Progression 2.

Single Limb Stance

Stand next to sturdy chair with your feet hip width apart. Gently hold on to the chair with both
hands and balance on one leg. Try to hold this for a few seconds before switching to the other
foot. Work up to 45-60seconds.
Progression 1: Hold chair with one hand. Then progress to no hands. Working up
to 45-60 seconds.
Progression 2: Holding the chair with one or two hands, close eyes and hold
single limb stance for a few seconds. Working up to 45-60 seconds.

Tandem Stance
Stand with your feet touching. Hold your arms out in a T position. Step forward touching the
heel of your shoe to the opposite toes. Try to hold this position for 3-5 seconds. Then reverse the
step and hold. Perform 8 repetitions on each leg.
Progression 1: Same as above, except hold arms straight up toward the ceiling
Progression 2: After stepping forward, close your eyes while holding the position
for 3-5 seconds.

Functional Squat
Stand in front of a chair with feet hip width apart. Hinging at the hip, slowly lower
yourself to the chair to a seated position. Try to stand up without using your hands.
Perform 2 sets of 10 reps
Theraband Rows
Place the knotted end of the theraband in the doorway and close the door securely. Make sure the
two loose ends are facing you. From a seated position, pull the theraband ends toward your
ribcage. Remember to concentrate on moving the shoulder blades toward each other in the
middle of the back. Perform 2 sets of 10 reps. To progress, use greater resistance band.

Theraband Chest Press

Wrap the theraband around your upper back. Hold the two loose ends slightly under your
underarms, with palms facing each other. Maintain elbows close to the ribcage as you bring the
arms in and then extend arms straight out. Perform 2 sets of 10 reps. To progress, use greater
resistance band.

Agility Ladder
Place agility ladder on the floor. Starting with both feet inside one box, walk over the ladder
placing each foot in the next empty box.
Program 2

Single Limb Stance on Balance Foam Surface

Stand on a balance foam, such as an Airex pad, with one hand holding a chair or wall if desired.
Feet should be hip width apart on the foam. Try to remain standing for 5-10 seconds
Progression 1: No holding on.
Progression 2: Close your eyes while trying to maintain balance for 5-10 seconds

Functional Stairs
Using stairs that contain a hand rail, practice going up and down 10 stairs.
Progression 1: increase to 20 stairs
Progression 2: hold a book while climbing stairs.

Single Arm Theraband Rows

Using the same theraband set up as Program 1, hold both theraband tails in one hand. From a
seated position, perform a single arm row. 2 sets of 10 repetitions.

Theraband Deadlift
Step on theraband with feet hip width apart. Criss cross the theraband
ends in each hand. Hinge from the to flex the hip, maintaining a neutral
spine. As you stand, squeeze your glute cheeks and abdominals. 2 sets
of 10 repetitions.
Shoulder Press
Sitting in a chair with a 2-3lb dumbbell in each hand, press the weight overhead. Maintain
neutral spine throughout movement. 2 sets of 10 repetitions.

Agility- Grapevine
Stand with feet together and arms at your side. Step across and in front of your left foot with the
right leg. Continue to step sideways, uncrossing the right leg. Reverse and cross your right leg
behind your left leg. Continue to step sideways, uncrossing the left leg. If you need extra help to
balance, keep your hands on a wall or railing in front of you. Perform 8-10 steps in each
direction.
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