What is Parkinson’s Disease?

Parkinson’s Disease

Parkinson’s disease (PD) is a progressive disorder in which nerve cells that produce the brain chemical dopamine gradually break down. Symptoms usually develop slowly over many years and can include tremor, slow movement, stiffness in the limbs, and problems with walking and balance.

How Common Is Parkinson’s Disease?

According to the Parkinson’s Foundation, about 1.1 million people in the United States are living with Parkinson’s disease, and nearly 90,000 are diagnosed each year. Men are about 1.5 times more likely than women to have PD. Age is the main risk factor, and only about 4% of people with PD are diagnosed before age 50 (1).

What Are the Early Signs of Parkinson’s Disease?

The Parkinson’s Foundation lists 10 common early warning signs. If you notice any movement-related signs, or a combination of signs, it’s a good idea to get a neurological evaluation (2).

Tremor. Shaking of a finger, thumb, hand or chin, especially while the limb is at rest, can be an early sign.

Small handwriting. Handwriting may become smaller or more crowded, called micrographia.

Loss of smell. Losing your sense of smell is a common early sign, and it can also affect taste.

Sleep problems. Thrashing in bed, restless legs, or acting out dreams during dream sleep can be early signs.

Stiffness and slowness. Stiffness in the arms, legs or body can be a sign of rigidity. Reduced arm swing while walking is often one of the earliest signs, along with shoulder stiffness or pain and slower walking.

Constipation. Occasional constipation is normal, but needing to strain with most or all bowel movements can be an early sign of PD.

Soft or low voice. A voice that becomes softer or quieter can be an early sign.

Masked face. A reduced range of facial expression, sometimes leaving a serious look even when you’re not upset, is common in PD.

Dizziness or fainting. Lightheadedness when standing up can reflect problems with blood pressure control, which can occur with PD.

Stooping. Leaning forward or hunching over can be a sign of changes in posture control.

What Are the Later Symptoms of Parkinson’s Disease?

The main movement symptoms include slow movement, called bradykinesia; tremor at rest, often looking like rolling a pill between the thumb and finger, which may lessen during movement; and rigidity, or stiffness of the muscles. Balance problems often develop later, raising the risk of falls.

Other movement symptoms can include dystonia, which is sustained, involuntary muscle tightening or twisting, and drooling. Some people develop dyskinesias, involuntary writhing or jerking movements, which are most often a side effect of long-term medication.

People with PD often walk with small, shuffling steps, and some develop festination, where steps become faster and shorter as if hurrying to catch up. Some experience freezing, a sudden inability to move the feet, especially when starting to walk, turning or going through doorways. Shuffling, festination and freezing all increase fall risk.

Reduced facial expression, called hypomimia, is common, along with a loss of automatic movements like blinking, smiling and swinging the arms while walking (3).

What Causes Parkinson’s Disease?

Parkinson’s disease is a protein buildup disorder. For reasons that aren’t fully understood, a misfolded protein called alpha-synuclein builds up in dopamine-producing cells. Once enough builds up, important cell functions begin to fail.

Every cell contains mitochondria, tiny energy factories that make the fuel cells run on. Two genes, PINK1 and Parkin, help detect damaged mitochondria and control their removal or repair. Alpha-synuclein buildup appears to interfere with this process, which can lead to mitochondrial failure. As alpha-synuclein accumulates, it clumps together into structures called Lewy bodies, which disrupt other cell functions. Eventually the cell fails and dies (4).

Research is also exploring a connection between the gut and Parkinson’s disease. Some studies have found that people with PD have a more permeable, or “leaky,” intestinal lining (5), along with differences in gut bacteria that may promote inflammation and oxidative stress. Some researchers believe Parkinson’s may begin in the nerves of the digestive tract in at least some people. One theory is that an overactive immune response to gut bacteria, together with a leakier intestinal lining, may trigger inflammation that contributes to alpha-synuclein buildup (6).

Another line of research suggests that misfolded alpha-synuclein may spread from cell to cell through the nervous system, somewhat like a prion. Prions are misfolded proteins that can cause other proteins to misfold. There is no evidence that Parkinson’s disease can be passed from person to person, but research supports the idea that, once it begins, PD may spread through the nervous system in a prion-like way (7).

In 2003, Braak and colleagues proposed that Parkinson’s may begin in the nose or digestive tract and then spread through the nervous system. This idea was based on finding Lewy bodies in the brain’s smell center and in the nerves of the gut. According to this model, the disease progresses through six stages, moving up through the brainstem and into the cerebral cortex (8).

Newer research builds on this idea. One theory suggests that in susceptible people, substances from gut bacteria may trigger alpha-synuclein clumps in the gut’s nervous system, which may then travel to the brainstem through the vagus nerve and continue spreading upward (9). These theories are still being studied.

What Happens in the Brain With Parkinson’s Disease?

Parkinson’s disease mainly affects cells that produce dopamine. The substantia nigra, an area in the upper brainstem, sends dopamine to the basal ganglia. The basal ganglia are a group of structures deep in the brain that act as both a gas pedal and a brake, helping start movements and stop them once they’re done. Dopamine helps the basal ganglia respond to the brain’s commands.

In a simplified view, the basal ganglia work through two main pathways. When dopamine is lost, the “go” pathway becomes less active, so movements become slower, harder to start and stiffer. Walking changes and steps get shorter. The “stop” pathway is also affected, which contributes to problems controlling unwanted movement, including tremor.

How Is Parkinson’s Disease Diagnosed?

Parkinson’s disease is usually diagnosed by a physician, typically a neurologist, based on symptoms and a neurological exam. Non-movement symptoms like loss of smell, constipation and sleep problems can help identify PD earlier, sometimes before movement symptoms appear (10).

In some cases, an MRI can show changes in the substantia nigra that support the diagnosis, and a special dopamine imaging scan can show reduced dopamine activity (11).

How Is Parkinson’s Disease Usually Treated?

There is no known cure for Parkinson’s disease, and treatment focuses on managing symptoms.

Medications that replace dopamine or help it last longer are the main treatment, and levodopa remains the most effective medication for movement symptoms (12). Medications can work very well, especially early on. Over time, their effects may wear off between doses, and many people eventually develop side effects such as dyskinesias. For some people whose symptoms are no longer well controlled by medication, deep brain stimulation (DBS) may help. DBS is a surgery that places small electrodes in the brain to help control movement symptoms (13). Regular exercise and physical, occupational and speech therapy are also important parts of care.

How the NeuroRescue Program Can Help

We cannot cure Parkinson’s disease or stop its progression. Our goal is to help you make the most of the function you have, with a focus on balance, walking, movement, eye movements, thinking and quality of life. Our care works alongside your neurologist and other providers, never in place of them. Never stop or change Parkinson’s medications without talking with your prescriber, since stopping suddenly can be dangerous.

Eye movements and balance. Much of the difficulty in Parkinson’s involves knowing where you are in space. Your brain combines signals from your muscles and joints, your inner ear and your eyes to build a picture of where you are. Your eyes constantly scan your surroundings using saccades, quick jumps from one point to another.

To move safely through the world, saccades need to be fast, accurate and quick to start. Because the basal ganglia help control saccades, they often become slow, less accurate and quick to tire in Parkinson’s. Research has linked these saccade problems to poor balance (14), difficulty turning (15) and freezing while walking (16). We use targeted saccade exercises with the goal of supporting balance, walking and stability.

Anti-saccades are a more complex type of eye movement, in which a person must hold back the urge to look at a new target and look the other way instead. Anti-saccades draw on the brain’s planning and self-control systems. Research shows that anti-saccades are affected in Parkinson’s, and these changes have been linked to problems with planning, reasoning and emotional control (17). We use anti-saccade exercises with the goal of supporting flexible thinking and emotional regulation.

Other therapies. Depending on your needs, your program may include vestibular rehabilitation, which has been studied for balance, walking and thinking (18); optokinetic visual stimulation, which has been studied for movement control and posture (19, 20); various forms of electrical stimulation, applied through the skin, which have been studied for balance, walking, eye movements, tremor, blood pressure regulation and swallowing (21, 22, 23); and virtual reality exercises, which have been studied for improving daily function and reducing fall risk (24).

Cognitive training. Parkinson’s disease often affects thinking skills such as attention, planning and processing speed. We use computerized cognitive training to exercise these skills. A review of studies found that computerized cognitive training led to small improvements in overall thinking skills in people with Parkinson’s disease (25).

Transcranial magnetic stimulation. TMS has been studied for improving movement, balance and mood in Parkinson’s disease (26). At our clinic, TMS is provided by our psychiatric mental health nurse practitioner, who will evaluate whether it’s appropriate for you.

Every person with Parkinson’s is different, and so is every NeuroRescue Program. Your plan is based on your test results and the specific factors of your case.

How the NeuroRescue Program Works

Your NeuroRescue Program begins with your Discovery Day. We start with a detailed history of your condition and your life on a timeline. This helps us understand the factors that may have contributed to where you are now, and identify related conditions that may be making it harder to move forward. When appropriate, we may also look at metabolic factors such as gut health, oxidative stress and mitochondrial function.

We measure how your visual, vestibular and balance systems are working through computerized analysis of your eye movements, inner ear reflexes and balance under different conditions. Our testing includes videonystagmography and saccadometry to measure several types of eye movements, the video head impulse test to measure inner ear reflexes, and CAPS computerized posturography to assess your balance under different sensory conditions. We also use NeuroSensoryMotor Integration testing to evaluate hand-eye coordination and cognition, and Virtualis testing to assess dynamic eye tracking and your perception of vertical in a virtual reality environment.

We combine this with a thorough physical and neurological exam of your sensory, motor, autonomic and cognitive systems. We also review any relevant lab work, imaging and prior testing, and integrate it with our findings.

Together, this helps us understand which parts of your nervous system are working well, which are struggling, and how quickly they tire. We use that information to design your personal NeuroRescue Program, aimed at supporting function and endurance in the systems that need it. Our testing also helps us decide when to push and when to let you rest.

We can’t bring back nerve cells that have been lost. What we can do is work with the pathways that remain, helping them work as efficiently as possible and work better together. Our goal is to help you stay as active, safe and independent as possible, for as long as possible.

Your Next Step

Living with Parkinson’s disease is challenging. While we cannot cure it, many symptoms can be managed, and function and quality of life can often be supported. To find out if the NeuroRescue Program is right for you, contact one of our patient care coordinators to schedule your Discovery Day.

It’s never too late to take the next step.

References

1. https://www.parkinson.org/understanding-parkinsons/statistics

2. https://www.parkinson.org/understanding-parkinsons/10-early-warning-signs

3. https://onlinelibrary.wiley.com/doi/full/10.1111/jnc.13691

4. https://molecularneurodegeneration.biomedcentral.com/articles/10.1186/s13024-020-00367-7

5. https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0028032

6. https://www.mdpi.com/1422-0067/19/6/1689

7. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5054685/

8. https://www.sciencedirect.com/science/article/abs/pii/S0197458002000659

9. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6558190/

10. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5636732/

11. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5636742/

12. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5372567/

13. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6587997/

14. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5091042/

15. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3247902/

16. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4867191/

17. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6261587/

18. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6297246/

19. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5348009/

20. https://www.sciencedirect.com/science/article/pii/S1808869415307138

21. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5766640/

22. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4388709/

23. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3528961/

24. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6463967/

25. https://researchers.westernsydney.edu.au/en/publications/computerized-cognitive-training-in-parkinsons-disease-a-systemati/

26. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4425190/

Previous
Previous

What is Progressive Supranuclear Palsy?

Next
Next

What is Multiple System Atrophy?