Most Parkinson’s resource sites group symptoms into two, sometimes three, broad categories. That structure is a helpful starting point, but at BetterChance Alliance, it’s not the finish line. PD doesn’t follow neat boundaries. Symptoms overlap, shift, and show up differently from person to person.Parkinson’s colors outside the lines.
That’s why BetterChance Alliance focuses on how symptoms actually appear in real life—connected, evolving, and personal.
Parkinson's Disease (PD) — Symptoms Categories Approach
Non-Movement Symptoms
1. Core Movement Symptoms
Bradykinesia (Slowed Movement) - A defining indicator of Parkinson’s Disease and required for diagnosis. Bradykinesia reflects difficulty starting, continuing, and scaling movement—not loss of strength. People often describe feeling slowed, stiff, or briefly :stuck.
Resting Tremor - Movement when the body is still. A rhythmic shaking that occurs when muscles are relaxed, most commonly affecting a hand, fingers, or leg. Occurs in approximately 70–80% of people with Parkinson’s, not a required for a Parkinson’s diagnosis. Note: This differs from essential tremor, which typically appears during movement rather than at rest.
Stride/Walking Gait Changes (Postural Instability)- Balance and walking are affected as coordination between posture and movement weakens. Stooped or forward-leaning posture, short, shuffling steps. Reduced or absent arm swing, difficulty turning or changing direction. Episodes of freezing, where the feet feel momentarily glued to the floor
Loss of automatic movements: Reduced ability to perform natural, unconscious actions such as blinking, smiling, or arm swing while walking.
2. Secondary Movement Symptoms
Speech changes: Speech may become softer (Hypophonia), slurred or poorly articulated (Dysarthria), rushed (Tachyphemia), and sound flat or monotone with reduced pitch and rhythm (Monoprosody).
Small or cramped handwriting (Micrographia)
Mask-like facial expressions changing very little or not at all. (Hypomimia)
Difficulty swallowing due to reduced throat muscle control (Dysphagia)
Drooling (due to reduced swallowing loss of facial muscle control, not excess saliva)
Movement (Motor) Symptoms
To start, we organize symptoms into three main categories: 1) Core Movement 2) Secondary Movement and 3) Non-Movement. To avoid a single catch-all grouping, where it’s far too easy to miss what matters, we further break Non-Movement into four distinct subcategories: a) Core Autonomic Functions b) Sensory Autonomic c) Cognition and d) Emotional/Mood.
This approach groups items in a more intuitive, practical way—making them easier to understand, recognize, and talk about in real life.
• Depression and anxiety
• Apathy (reduced motivation)
• Irritability
• Emotional fatigue
• Stress sensitivity
• Impulse-control symptoms (sometimes medication-related
These symptoms reflect brain chemistry changes, not personality or attitude.
Emotional/Mood
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Cognitive Indicators
• Slower processing speed
• Difficulty multitasking
• Trouble with concentration and focus
• Word-finding difficulty
• Executive function
changes (planning,
organizing, sequencing)
Note: Changes in thinking and processing — not emotional, not movement
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Sensory Autonomic
• Temperature and sweating regulation issues
• Pain sensitivity changes
• Tingling or discomfort without injury
• Sleep disorders, including:
- REM sleep behavior disorder (acting out dreams)
- Restless legs syndrome
- Periodic limb movement disorder (PLMD)
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Core Autonomic
-Blood pressure regulation issues (orthostatic hypotension — dizziness when standing)
• Digestive changes
(constipation, slowed gut movement)
• Bladder changes (Urinary urgency or incontinence)
• Temperature and sweating regulation issues
• Sexual function changes
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Research increasingly suggests that these symptoms can show up very early—often years or even decades before the more familiar movement symptoms begin.
Subcategorized t0 mAke them easier to recognize,
Commonly recognized risk factors include age, genetics, gender and certain environmental exposures. Next, we take a slightly deeper look at what researchers understand about each—and what those factors may mean over time—without pretending the brain ever follows a simple rulebook.
What are the risk factors of developing PD?
you might be wondering...
Parkinson’s Disease develops differently from person to person, and it doesn’t follow one single pattern. Some people notice gradual changes over time, while others experience symptoms in a different order or at a different pace.
While certain factors can increase the likelihood of developing Parkinson’s, having one or more of these does not mean someone will develop the disease, it simply means the odds may be slightly higher. Risk factors can offer helpful clues, but they are not a prediction.
Age
Risk increases with age. Parkinson’s most often begins after age 50, with the average age of onset between 60-70. It can occur earlier, but this is uncommon. When symptoms begin before age 50, it is referred to as early-onset Parkinson’s Disease.
Genetics
Having a first-degree relative (such as a parent or sibling) with Parkinson’s does increase risk, but the overall likelihood remains low unless multiple family members are affected or a known genetic mutation is present.
Gender
Men are more likely than women to develop Parkinson’s disease. The reasons for this difference are not fully understood, but the pattern is consistent across large studies.
Environmental Exposures
Long-term exposure to certain environmental toxins — particularly some pesticides and herbicides — has been associated with a slightly increased risk. This does not mean occasional exposure causes Parkinson’s, but some substances have shown consistent patterns that warrant ongoing research.
The Causes of Parkinson's
Parkinson’s disease is classified based on what is known — or not known — about its underlying cause. Broadly, it falls into three categories: genetic, idiopathic, and induced Parkinsonism.
What Causes Parkinson’s Disease?
Parkinson’s Disease can be inherited, though this accounts for only about 10% of all cases. Researchers have identified at least seven genes linked to Parkinson’s, with several associated with early-onset disease. Certain genetic forms may also have distinctive features or progression patterns.
Even in families with known mutations, not everyone who carries the gene will develop Parkinson’s, suggesting that genetics alone are not always the full explanation.
Genetics in Parkinson’s?
Most cases of Parkinson’s are classified as idiopathic, meaning there isn’t one clear, identifiable cause. The word idiopathic comes from Greek and loosely translates to “a disease of its own.”
(if you’re a fan of My Big Fat Greek Wedding… we do not recommend squirting Windex on this one. So there you go.)
Current research suggests Idiopathic Parkinson’s involves abnormal processing of a protein called α-synuclein. When this protein misfolds, it can accumulate inside nerve cells, forming clumps known as Lewy bodies. Over time, these clumps interfere with normal cell function and damage neurons—particularly dopamine-producing cells, which play a critical role in movement and coordination. critical role in movement and coordination.
What Idiopathic Parkinson's Mean?
Possible causes include:
- Medications
What Does Induced Parkinsonism Mean?
• Inflammation or infection
Brain inflammation (Encephalitis) can sometimes lead to Parkinsonism.
• Toxins and poisons
Exposure to substances such as manganese dust, carbon monoxide, welding fumes, or certain pesticides can lead to Parkinsonism (Parkinson’s-like symptoms). One rare example is MPTP, a substance once found in illegally manufactured “synthetic heroin.” While no environmental exposure has been proven to directly cause Parkinson’s Disease, some remain on researchers’ “strongly suspicious” list.
Other Items Falling Under Induced Parkinsonism?
Not because it’s something most people will ever encounter, but because rare cases in the 1980s revealed that MPTP—after converting to its toxic form, MPP+—selectively destroys dopamine-producing neurons, the same cells affected in Parkinson’s disease. This discovery provided critical insight into the disease’s biology and helped advance research and treatment development.
Why mention MPTP?
Environmental Factors & PD Risk?
- Insecticides: Permethrin, β-Hexachlorocyclohexane•
- Herbicides: Paraquat, 2,4-D
- Fungicide: maneb
- Industrial solvent: Trichloroethylene (used in dry cleaning and degreasing)
- Heavy metals like Manganese
While accidents, falls, or sudden physical or emotional shock do not directly cause Parkinson’s disease (PD) in most cases, they can serve as significant triggers. In people who are already vulnerable, these events may accelerate the onset of symptoms or worsen existing ones, acting as a tipping point after years of quiet, preclinical changes in the brain.
Research suggests that major trauma or shock can place added strain on already-compromised dopamine neurons, increase inflammation, and reduce the brain’s ability to compensate.
Can a bad fall, accident or shock cause PD?
While stress doesn't directly cause Parkinson's Disease (PD) inmost cases, it can be a significant trigger, accelerating its onset or worsening symptoms, especially in vulnerable individuals, acting as the "last straw" after years of preclinical changes due to its effects on dopamine neurons and inflammation. Research suggests chronic stress increases brain cell loss, elevates damaging stress hormones (like glucocorticoids), and primes the brain for neurodegeneration, making stress a potential risk factor alongside genetics and environmental toxins.
Can Stress Cause PD?
Sleep Apnea does not directly cause Parkinson’s. However, growing scientific evidence shows a meaningful connection between untreated obstructive sleep apnea (OSA) and an increased risk of developing Parkinson’s over time.
Research summarized by The American Journal of Managed Care indicates that untreated OSA is associated with roughly a 30–60% higher risk of Parkinson’s compared with people without sleep apnea. These findings reflect a moderate but clinically important increase in risk, not a certainty.
Scientists believe this relationship is driven by repeated drops in oxygen, disrupted sleep, inflammation, and ongoing stress on brain cells—conditions that may accelerate underlying neurodegenerative changes rather than directly cause the disease.
The encouraging news is that OSA is a modifiable risk factor. Evidence suggests that people who receive effective treatment—most commonly CPAP therapy—show a reduced or no significant increase in Parkinson’s risk. This makes early recognition and treatment of sleep apnea an important opportunity for proactive brain health.
More broadly, sleep disorders such as OSA and REM Sleep Behavior Disorder are now understood as early, non-motor features of Parkinson’s disease, sometimes appearing years before movement symptoms
