Parkinson's Disease

An Overview of Parkinson's Disease

Parkinson's disease develops as a result of the death of dopamine-producing nerve cells in the brain. Dopamine is a vital neurotransmitter (chemical messenger in the brain) that helps regulate muscle activity. So when dopamine is depleted in the brain, symptoms like shaking, stiffness, and walking difficulties occur.

While Parkinson's disease used to be considered solely a movement (motor) disorder, experts now recognize that it also causes non-motor related symptoms like sleeping problems, constipation, and loss of smell.

What's interesting is that these symptoms may actually predate the motor symptoms by many years, even decades.

It's important to understand that Parkinson's disease is a complex disease. But by learning small tidbits of knowledge about this brain disorder, you are already on your way to living well (or helping a loved one) live well with it. 

Cause of Parkinson's Disease

While the precise cause of a person's Parkinson's disease is usually unknown, experts believe that it results from a complex interaction between one's genes and his or her environment.

Examples of environmental exposures that may trigger the development of Parkinson's disease in a genetically vulnerable person are pesticides or rural living. Other risk factors for Parkinson disease are increasing age and gender (Parkinson's disease is more common in men). 

Symptoms of Parkinson's Disease

The symptoms of Parkinson's disease can be subtle early on—in fact, they may even go unnoticed. But eventually the symptoms slowly worsen with time.

Motor Symptoms in Parkinson's Disease

Four hallmark motor symptoms of Parkinson's disease are:

  • Tremor
  • Bradykinesia (a slowness of movement)
  • Rigidity
  • Postural instability (sense of imbalance)

    Tremor in Parkinson's disease is classically called a "pill-rolling" tremor because of the way it appears—as if a person is rolling a pill or other tiny object between his or her thumb and index finger. It's also described as a resting tremor because it occurs when a body part (like the hand) is relaxed and resting. When a person engages in purposeful movements, like reaching for a glass, the tremor decreases or disappears. Tremor can be found in other parts of the body too, like the foot or jaw, and is usually worsened by stress.

    It's interesting to note that while resting tremor occurs in the vast majority of those with Parkinson's disease, it is not present in everyone. 

    Bradykinesia describes a person's decreased ability to move. As you can imagine, this can be particularly disabling. A person may progress from difficulty using his or her fingers (for example, opening a jar or typing) to difficulty using their legs, leading to a shuffling gait with short steps. 

    Rigidity refers to muscle stiffness and resistance to muscle relaxation. A person with rigidity may not swing their arms much when walking, or he or she may tend to flex or bend forward.

    Rigidity can be painful, and this can also contribute to difficulty moving, especially walking.

    Another symptom of Parkinson's disease is postural instability—a sense of imbalance when standing up. This symptom usually arises later on in the course of Parkinson's disease. In a person with postural instability, a small poke on the arm can lead to them falling over. 

    There are many other motor-related symptoms in Parkinson's disease, and their presence is variable, meaning not everyone experiences the same symptoms or has them to the same degree. Some of these motor-related symptoms include:

    • Decreased eye blinking
    • Reduced facial expressions
    • Speech and swallowing problems
    • Excessive saliva production
    • Freezing episodes—where a person feels like their feet are superglued to the floor or their bottom is frozen to a chair

    Non-Motor Symptoms in Parkinson's Disease

    As research into Parkinson's disease progresses, experts are now focusing more and more on non-motor related symptoms. These symptoms are often more debilitating for a person than their motor symptoms, and they can start years earlier.

    Examples of non-motor symptoms in Parkinson's disease include:

    • Hallucinations (usually visual) and/or delusions
    • Mood disorders like depression, anxiety, and apathy (loss of interest and emotion)
    • Sleep problems and daytime tiredness
    • Cognitive problems and dementia
    • Autonomic dysfunction (for example, a drop in blood pressure when standing up or constipation)
    • Sensory disturbances like numbness and tingling or pain 
    • Skin problems (for example, seborrheic dermatitis)
    • Loss of sense of smell

    Diagnosis of Parkinson's Disease

    The diagnosis of Parkinson's disease requires a careful and thorough evaluation by a doctor, usually a neurologist, as there is no slam dunk blood test or brain imaging test for it. While the diagnosis is straightforward in some people, it may be more challenging in others, especially since there are a few other neurological health conditions that share similar symptoms with Parkinson's disease. 

    If your doctor suspects Parkinson's disease, he will ask several questions about sleep, mood, memory, walking problems, and recent falls.

    He will also perform a physical examination to check reflexes, muscle strength, and balance. Do not be surprised if imaging tests or blood tests are ordered to rule out other medical conditions. 

    There are also specific criteria a doctor follows to diagnose Parkinson's disease. For example, one criterion that supports a diagnosis of Parkinson's disease is if a person with Parkinson-like symptoms has a marked improvement in their symptoms after taking levodopa (a medication used in the treatment of Parkinson's disease).

    While there is no cure for Parkinson's disease, the good news is that there are a number of treatment options to ease symptoms so you or your loved one can live well with it.

    Treatment of Motor Symptoms 

    Deciding when to start a medication for motor symptoms is not always clear cut either—it depends on the person and how debilitating their symptoms are. In fact, you may be surprised to learn that in the early stages of Parkinson's disease, medication may not be needed. 

    Carbidopa-levodopa, which goes by brand names Sinemet or Parcopa, is the primary and most effective Parkinson's medication. Levodopa is converted into dopamine in the brain, which helps restore muscle control. Carbidopa makes levodopa more effective by preventing it from converting into dopamine outside of the brain.

    The downside of this otherwise very effective medication is that once a person has been on it for years, it may not be as good at managing motor symptoms—this is called the "wearing off" effect. In addition, movements that are out of your control like muscle spasms or jerking (called dyskinesia) may occur after prolonged use of levodopa.

    Dopamine agonists like Mirapex (pramipexole) and Requip (ropinirole) stimulate dopamine receptors—docking sites—in the brain, tricking the brain into thinking it has the dopamine it needs to get the body to move. Dopamine agonists are less effective than levodopa, and they do have a number of potential side effects such as visual hallucinations, sleep attacks (acute sleepiness), and compulsive behaviors like gambling, eating, shopping, or sexual behavior.

    That being said, dopamine agonists are sometimes used in the earlier stages of Parkinson's disease, postponing the need for levodopa until later on in the disease course. This can help prevent long-term complications of levodopa like the "wearing off" effect and out-of-control body movements. 

    Monamine oxidase inhibitors (MAO-B inhibitors) include Eldepryl, Emsam, and Zelapar (selegiline) and Azilect (rasagiline), which treat motor symptoms by inhibiting the enzyme that normally inactivates dopamine in the brain. This allows active dopamine to hang around in the brain more.

    The downsides of monamine oxidase inhibitors is that they are not as effective as levodopa for people with Parkinson's disease, and they can interact with other medications, like antidepressants.

    The upside is that they can sometimes provide benefit in suppressing motor symptoms in the earlier stages of Parkinson's disease, essentially buying a person some time before having to start levodopa. 

    COMT inhibitors like Comtan (entacapone) and Tasmar (tolcapone) work by increasing the effect of levodopa in the brain (so they are taken with levodopa). They are used to treat people who experience the "wearing off" effect of being on levodopa long-term. Monitoring of liver blood tests is needed if a person is on Tasmar (tolcapone).

    Anticholinergics like Artane (trihexyphenidyl) and Cogentin (benzotropine) are prescribed to minimize the discomfort of tremor in people with Parkinson's disease. They work by increasing acetylcholine in the brain.

    The downside is that anticholinergics have numerous potential adverse effects like blurry vision, dry mouth, retaining urine, constipation, and confusion (especially in older adults). Because of this, they are reserved for those individuals with Parkinson's disease under the age of 70. 

    Symmetrel (amantadine) is an antiviral medication that is used in early Parkinson's disease to manage mild tremor and rigidity. Potential side effects include dry mouth, constipation, skin rash, ankle swelling, visual hallucinations, and confusion. 

    Treatment of Non-Motor Symptoms

    Aside from the movement problems associated with Parkinson's disease are the often less visible symptoms like sleep problems, cognitive problems, and mood changes, which can negatively impact a person's quality of life. The good news is that there are excellent therapies to address them. 

    For example, depression is common in Parkinson's disease, but it can be treated with traditional antidepressants, like selective serotonin reuptake inhibitors. For dementia (thinking and memory problems), the skin patch Exelon (rivastigmine) may be prescribed.

    Hallucinations and psychosis can be especially disturbing for a person (and their loved ones) with Parkinson's disease. To address this, a neurologist may stop or decrease the dose of their Parkinson's medication (for example, levodopa). For more serious cases of hallucinations, an antipsychotic medication may be prescribed. 

    Rehabilitation therapies like speech, occupational, and physical therapy are also commonly used to improve quality of life in Parkinson's disease.

    Deep Brain Stimulation

    Deep brain stimulation is reserved for those with advanced Parkinson's disease whose motor symptoms are not effectively treated anymore with medication. It is particularly effective for people with persistent, disabling tremors, and those with uncontrollable movements (called dyskinesia) or fluctuations ("waxing and waning" symptoms), which are complications of using levodopa long-term. 

    Deep brain stimulation entails a neurosurgeon implanting a wire deep within the brain. This wire is connected to a battery-operated device called a neurostimulator, which is placed under the skin near the collarbone. Electrical pulses delivered from the neurostimulator (controlled by the patient) is believed to alter the intricate nerve pathways in the brain that control movement (so normal movements are produced instead of abnormal ones, like tremor). 

    It's important to understand that this surgical treatment is not a cure and does not stop a person's Parkinson's disease from progressing. There are also serious risks involved, warranting a thoughtful discussion with a person's neurologist, surgeon, and family before undergoing it. 

    A Word from Verywell

    Parkinson's disease is a complex neurodegenerative ("dying of brain cells") disorder that affects not only how a person moves, but also how they think, feel, sleep, and even smell. While these symptoms can be disabling, the good news is that there are effective ways to reduce their impact on your or your loved one's life. 


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    Wagle Shukla A, Okun MS. Surgical treatment of Parkinson's disease: patients, targets, devices, and approaches. Neurotherapeutics. 2014 Jan;11(1):47-59.

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