What is Parkinson’s Disease?

Jul 28

Parkinson’s disease, or PD, is a progressive disorder that causes neurons that produce the neurotransmitter dopamine to degenerate. Symptoms of Parkinson’s disease can develop slowly over many years, which can include tremor, slowness of movement, limb stiffness, and problems with gait and balance.

How Common is Parkinson’s Disease?

According to the Parkinson’s Foundation, around 930,000 Americans live with Parkinson’s disease. Roughly 60,000 people are diagnosed with PD each year. Men are 1.5 times more likely to develop PD than women, and 96% of cases develop after age 50 (1).

What are the Early Signs of Parkinson’s Disease?

There are 10 widely accepted early signs of Parkinson’s disease. The presence of any motor signs, or any combination of more than one sign should lead you to have a proper neurological evaluation.

Tremor involving the finger, thumb, hand, or chin can be an early sign of Parkinson’s disease. Tremors present when the limb is at rest are most commonly signs of PD.

Small Handwriting, or micrographia, can be indicative of Parkinson’s disease. Small letters or crowded words is a common early sign.

Loss of smell is a very common early sign. This can also manifest as a loss of taste.

Sleep difficulties involving thrashing in bed, restless legs, or acting out dreams while in deep sleep can indicate PD.

Stiff muscles in the arms, legs, and body can be a sign of rigidity from loss of dopamine production. A loss of arm swing is often the earliest sign, along with stiffness or pain in shoulders and slowness of gait.

Constipation can be a sign that dopamine producing neurons in the gastrointestinal tract are starting to fail. Occasional constipation is normal, but straining with most or all bowel movements can be an early PD sign.

Soft or low voice can indicate that PD is affecting brainstem control of vocal cords.

Loss of facial expression, also called masked face, can imply that PD is affecting the brainstem’s ability to regulate facial muscle tone. A fixed, serious expression at all times is often a hallmark of PD.

Dizziness or fainting can be a sign of dysautonomia, in which blood pressure regulation is decreased as PD advances.

Stooping or hunching over is called camptocormia, a sign of breakdown in the systems that regulate posture with advancing Parkinson’s disease (2).

What are the Later Symptoms of Parkinson’s Disease?

Movement symptoms include slowness of movement called bradykinesia. People living with PD also usually note a tremor, often one that looks like an attempt to roll a pill between the finger and thumb when at rest, and goes away during movement. They often experience rigidity, a stiffness of muscles with all directions of movement. People also often develop postural instability later in the disease progression, leading to balance problems and increased fall risk.

Additional motor symptoms can involve dystonia, which is a repetitive twisting or tightening of a muscle. People can experience uncontrolled drooling, or involuntary writhing movements of facial muscles called dyskinesia.

People living with PD often show a festination gait, where they demonstrate small, shuffling steps. They may also show freezing when walking or going through doorways. Festination and freezing increase a person’s fall risk.

They also commonly show hypomimia, or loss of facial expression, and a loss of automatic movements like blinking, smiling, or swinging arms when walking.

What Causes Parkinson’s Disease?

Parkinson’s disease is a protein aggregation disorder. For reasons that are not well understood, a misfolded protein known as alpha-synuclein begins to accumulate in dopamine-producing cells. When enough of this protein builds up, a number of important cellular functions become compromised.

All of our cells contain tiny structures called mitochondria. These are energy factories that make ATP, the molecule that powers cellular chemical reactions. A pair of important genes, PINK1 and Parkin, function to detect damage to mitochondria and control their removal or regeneration. Alpha-synuclein buildup impairs the function of these genes, which leads to mitochondrial failure. As alpha-synuclein builds up in the cell it begins to clump together to form Lewy bodies, which interfere with other cellular functions. Ultimately the alpha-synuclein buildup causes the cell to fail and die (3).

New studies indicate that there is a direct connection between intestinal permeability, gut bacteria, and PD. Research shows that Parkinson’s patients have “leaky guts,” with increased permeability of the intestinal wall to dietary proteins and inflammatory chemicals. They also show abnormal gut bacteria, which produce endotoxins that further damage the intestinal wall and lead to oxidative stress.

Leaky gut appears to be directly linked with the production of alpha-synuclein in the dopamine producing cells of the enteric nervous system, where most researchers now think is where Parkinson’s disease first develops (4). It appears that an overstimulation of the immune system due to gut dysbiosis and/or small intestinal bacterial overgrowth, together with higher intestinal barrier permeability, may provoke local and systemic inflammation. This promotes the activation of a direct neuroinflammation response that ultimately triggers the development of alpha-synuclein pathology (5).

There is another emerging body of research that supports the possibility that PD is based on the spread of a prion. Prion is short for proteinaceous infectious particle. Prions can self-transform their shape and propagate through the nervous system. They can be transmitted from cell to cell, between individuals, and even between animals of different species. Prions are the cause of particularly severe neurodegenerative conditions such as Mad Cow Disease.

While no research currently demonstrates that Parkinson’s disease is a transmissible condition between individuals, there is good support that once established, PD spreads through the nervous system in a similar manner to prion diseases (6).

Braak proposed a theory in 2003 that stated Parkinson’s disease started with a foreign body entering the nervous system through the nose or GI tract, then spreading through the body. This was based on the presence of Lewy bodies found in the olfactory bulb and the enteric nervous system of the GI tract in PD patients. From there, the disease would progress through six stages as it moved higher in the brainstem and forward through the cerebral cortex (7).

Recent studies appear to unify the concept that gut bacteria play an important role in the development and progression of Parkinson’s disease. Research now implies that in susceptible individuals, gut toxins from bacterial dysbiosis can induce the formation of α-synuclein aggregates in the enteric nervous system. Once established, they can be transmitted in a prion-like manner to the central nervous system through the Vagus nerve. They will then begin to form alpha-synuclein aggregates in the lower brainstem and the disease will continue to progress higher in the nervous system (8).

What is Going on in the Brain with Parkinson’s Disease?

In Parkinson’s disease, the production of Lewy bodies primarily affects cells that produce dopamine. The Substantia Nigra Pars Compacta is an important region in the upper brainstem that produces dopamine that supplies the basal ganglia. These are a complex group of nuclei that live between the brain and the brainstem, and function as both the gas and brake pedals for the brain. The basal ganglia are necessary to first turn on every movement, then once it has been completed, to turn it back off. Dopamine from the Substantia Nigra makes the basal ganglia sensitive to the brain’s commands. In essence, the basal ganglia need dopamine to hear what the brain is asking it to do.

When dopamine production is lost, the basal ganglia’s direct pathway is first to be affected. This functions as the gas pedal, and when this is affected movements become slow and difficult to initiate, and the body becomes stiff. Often the first manifestation of this is a stiff or painful shoulder or hip. Gait patterns will change and stride length will shorten. As the disease progresses, the indirect pathway becomes involved, and the brain’s foot slides off the brake pedal. It becomes difficult to stop or suppress unwanted movement, and tremors and dystonia begin to manifest.

How is Parkinson’s Disease Diagnosed?

Parkinson’s disease is in most cases a clinical diagnosis. When more than one of the primary symptoms of PD are present, a provider will usually refer to a neurologist, where a full neurological examination will generally reveal other findings that confirm the disease (21).

In some cases, and MRI scan can show patterns of cell loss in the substantia nigra that support the diagnosis. A dopamine tracer scan can also be employed to show failure of dopamine pathways (22).

How is Parkinson’s Disease Usually Treated?

There is no known cure for Parkinson’s disease. Most therapy focuses on controlling symptoms.

People are generally treated with medications that either slow the breakdown of dopamine, or function as dopamine replacement. These tend to control tremors for a time, however they have a significant side effect profile, and ultimately lead to the development of secondary dyskinesias (23). When people stop responding to medications, deep brain stimulus may be helpful. This requires brain surgery to implant tiny electrodes in the basal ganglia. This again will lose effectiveness over time (24).

How is the NeuroRescue Program Different?

While we cannot cure Parkinson’s disease, we employ a host of advanced therapies and technologies that can help improve the function of your remaining systems. By doing so, we can often help restore your mobility, reduce your tremor, improve your balance and gait, and enhance your quality of life.

Much of what happens in PD is related to the inability to properly localize yourself in the environment. Your brain makes sense of where you are in the world through inputs from your muscles and joints, inputs from your inner ear, and inputs from your eyes. The eyes are constantly scanning the world to provide the brain with a visual map of the surrounding space. It does this with saccades, which are fast eye movements from target to target.

In order for you to move through and interact with the world, you first need to know where the world is. This requires that saccades are fast, accurate, stable, and have very quick reaction times. As the basal ganglia are involved in saccades, all of these functions break down with PD. Saccades become slow, lose accuracy, and are easy to fatigue. Research shows that the breakdown in saccades seen with PD leads to postural instability (9), impairs the ability to turn (10), and leads to freezing of gait (11). We find that by rehabilitating saccades in a very precise manner, we can often improve balance, gait, and postural stability.

Another more complicated eye movement is called an anti-saccade, where a target is presented, and a person needs to inhibit the reflex to look at the target and instead consciously choose to look in the other direction. Anti-saccades are involved in a number of executive functions, and these give rise to foundational cognitive processes. Research shows that anti-saccades break down in Parkinson’s disease, leading to problems with planning, reasoning, and emotional regulation (12). We find that by rehabilitating these eye movements we can often restore some of the cognitive flexibility and emotional regulation lost to this disease.

There are a host of other therapies that we engage in with our Parkinson’s disease patients. All of these have different functions and allow us to rehabilitate specific capacities. These range from vestibular rehabilitation to improve balance, gait, and cognition (13), to visual optokinetic stimulation to improve motor control and postural stability (14,15). They include a number of different types of electrical stimulation to improve cognition, eye movements, balance, gait, tremor, blood pressure regulation, and even swallowing (16,17,18). They even include therapies such as transcranial magnetic stimulation to improve motor function, emotional regulation and balance (19), and virtual reality exercises to improve the ability to function in the world and decrease fall risk (20).

No two Parkinson’s disease presentations are alike, and the same holds true for the NeuroRescue program. A cookie-cutter approach will be doomed to fail in a condition as complicated as PD. All of our therapy protocols are tailored to the unique needs of the individual.

How Does the NeuroRescue Program Work?

We design your unique NeuroRescue Program to be among the most comprehensive diagnostic and therapeutic protocols available today. We create individual NeuroRescue Programs based on a comprehensive analysis of every relevant neurological system and pathway, using gold-standard, cutting edge neurodiagnostic technologies and examination procedures and state-of-the-art therapies.

We begin with your Discovery Day, wherein we perform a comprehensive history of not only your condition, but your life on a timeline. This allows us to dive deeply into your case and see all of the factors that led to where you are now. It helps us uncover hidden problems and associated conditions that may be making it difficult for you to move your recovery forward.

In the case of Parkinson’s disease, this requires a deep dive into the gut microbiome, intestinal wall permeability, mechanisms of oxidative stress and mitochondrial failure, and many other factors that can be provoking your issues.

Our examination allows us to identify the areas and pathways of your brain that have been impacted by your Parkinson’s disease. We begin by precisely quantifying the function of your visual, vestibular, and proprioceptive systems through computerized analysis of your eye movements, your inner ear reflexes, and your balance in a host of different sensory conditions.

We employ technologies including Videooculography and Saccadometry to measure several classes of eye movements. We use Video Head Impulse Testing to measure the function of your inner ear, and Computerized Dynamic Posturography to assess your balance in different sensory conditions.

We use NeuroSensoryMotor Integration testing to evaluate hand-eye coordination and cognition, and Virtualis testing to assess dynamic eye tracking and perception of vertical in a virtual reality environment.

We combine all of this with a comprehensive physical and neurological examination of your sensory, motor, autonomic, and cognitive systems. We review any relevant laboratory testing, radiological imaging, and prior neurodiagnostic testing, and integrate that information with our findings.

We use this information to identify which parts of your brain are working properly, which systems are struggling, and the precise point at which your systems fatigue.

We can then design a NeuroRescue Program that is unique and specific to your brain, and yours alone. Your NeuroRescue Program works to rejuvenate and reintegrate the damaged neurons and pathways in your brain. It works to improve energy, endurance, and functional capacity within your fragile systems.

We use our technologies and procedures to not only see what we need to address, but also when it is time to stop and let you rest. We address your impaired neurological function from multiple angles of therapy, and provide metabolic support to improve neurological recovery.

While we cannot bring back neurons that have been lost to Parkinson’s disease, your NeuroRescue Program allows us to take the pathways that remain and maximize their efficiency and endurance. And by focusing on the integration of systems, we can do more than just get pathways working better, we can get them working together again. This gives us our best opportunity to help you live a healthy, vibrant, and fulfilling life.

Your Next Best Step:

Living with Parkinson’s disease is challenging. While we cannot offer a cure for the condition, many of the symptoms can be manageable, function can often be enhanced, and quality of life may be significantly improved. To see if the NeuroRescue Program is right for you, contact one of our patient care coordinators to schedule your Discovery Day.

And remember, it’s never too late to start getting better.