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Diagnosis
 

There is no “one way” to diagnose Parkinson’s disease (PD). However, there are various symptoms and diagnostic tests used in combination. In this section, you will learn how PD is diagnosed as well as the various Parkinsonism syndromes that often mimic the symptoms of PD. 

 

 

How does your doctor make a PD diagnosis?
 

 

One of the most important things to remember about diagnosing PD is that there must be two of the four main symptoms present over a period of time for a neurologist to consider a PD diagnosis. 
 

Four Main Motor Symptoms of PD:

  • Shaking or tremor
  • Slowness of movement, called bradykinesia
  • Stiffness or rigidity of the arms, legs or trunk
  • Trouble with balance and possible falls, also called postural instability
     

How does your doctor make a PD diagnosis?
 

The bedside examination by a neurologist remains the first and most important diagnostic tool for patients suspected of having PD. When questions arise, some newer imaging modalities such as PET and DAT scans may aid diagnosis, when performed by an expert in neuroimaging. DATscan is FDA-approved for differentiating PD from essential tremor, but it cannot distinguish between PD and parkinsonian subtypes. A neurologist will make the diagnosis based on:

  • A detailed medical history and physical examination.
  • A detailed history of your current and past medications, to make sure you are not taking medications that can cause symptoms similar to PD.
  • A detailed neurological examination during which a neurologist will ask you to perform tasks to assess the agility of arms and legs, muscle tone, your gait and your balance. 
  • You may notice that a neurologist records your exam into a table, called United Parkinson’s Disease Rating Scale (UPDRS). UPDRS is a universal scale of PD symptoms and it was created to comprehensively assess and document the exam of the patient with PD and be able to compare it with patient’s future follow up visits, or to communicate about the progression of the PD symptoms in each patient with other neurologists. 
  • Visit the Movement Disorders Society for their version of the UPDRS .
  • The response to medications (that imitate or stimulate the production of Dopamine) causing a significant improvement in symptoms is how the diagnosis of PD is made clinically.

 

Want to Learn More?
 

 

Medical content reviewed by: Nina Browner, MD—Medical Director of the NPF Center of Excellence at the University of North Carolina at Chapel Hill in North Carolina and by Fernando Pagan, MD—Medical Director of the NPF Center of Excellence at Georgetown University Hospital in Washington, D.C.

 

 

Can you have Parkinsonism without having

PD?

 


 

YES. Parkinsonism is an inclusive term, which means that the patient has symptoms similar to Parkinson’s disease (like tremor, rigidity, slowness of movements and balance problems), although a doctor is not sure whether those symptoms are due to neurodegeneration of dopamine neurons in the substantia nigra. A number of patients with Parkinsonism do not have PD. Only 85% of all Parkinsonian syndromes are due to Parkinson’s disease. Certain medications, vascular problems, and other neurodegenerative diseases can cause the symptoms similar to Parkinson’s disease. In fact, early in the disease process it may be difficult to know whether a patient has typical Parkinson’s disease or a syndrome that mimics it. The development of additional symptoms and the subsequent course of the disease generally points to the correct diagnosis.

Did you know that you could have symptoms of Parkinson’s without having PD?

A variety of blood tests and a brain scan will be done to rule out other conditions.


Neurodegenerative diseases causing Parkinsonism are commonly grouped together under the category of Atypical Parkinsonism or Parkinsonism – plus syndromes. The plus part means, that in addition to expected symptoms of PD, patients have some atypical symptoms as well. Atypical Parkinsonism should be considered particularly in patients with:

  • Poor response to dopamine
  • Early loss of balance
  • Prominent intellectual changes (dementia)
  • Rapid onset or progression 
  • Conspicuous postural hypotension, urinary and bowel incontinence
  • Little or no tremor.

 

Want to Learn More?
 

Medical content reviewed by: Nina Browner, MD—Medical Director of the NPF Center of Excellence at the University of North Carolina at Chapel Hill in North Carolina and by Fernando Pagan, MD—Medical Director of the NPF Center of Excellence at Georgetown University Hospital in Washington, D.C.

 

 

What are the different types of atypical

Parkinsonism Syndromes?
 

 

I. Drug-induced Parkinsonism

  • Side effects of some drugs, especially those that affect dopamine levels in the brain, can actually cause symptoms of Parkinsonism.
  • Although tremor and postural instability may be less severe, this condition may be difficult to distinguish from Parkinson’s disease.
  • Medications that can cause the development of Parkinsonism include:
    • Antipsychotics
    • Metaclopramide
    • Reserpine
    • Tetrabenazine
    • Some calcium channel blockers
    • Stimulants such as amphetamines and cocaine
    • Usually after stopping those medications Parkinsonism gradually disappears
    •  

II. Progressive Supranuclear Palsy (PSP)

  • PSP is one of the more common forms of atypical Parkinsonism.
  • Symptoms of PSP usually begin after age 50 and progress more rapidly than PD.
  • These symptoms include: imbalance, frequent falls, rigidity of the trunk, voice and swallowing changes and (eventually) eye-movement problems including the ability to move eyes up and down.
  • Dementia develops later in the disease. There is no specific treatment for PSP.
  • Dopaminergic medication treatment is often tried and may provide some benefit.
  • Other therapies such as speech therapy, physical therapy, and antidepressants are important for management of patients with PSP.
  • No laboratory/brain scan testing exists for PSP. In rare cases, some patients may have shrinking of a particular part of the brain, called the “Pons”, which can be seen on an MRI of the brain.
  •  

III. Corticobasal Degeneration (CBD)

  • CBD is the least common of the atypical causes of Parkinsonism
  • CBD develops after age 60 and progresses more rapidly than PD.
  • The initial symptoms of CBD include asymmetric bradykinesia, rigidity, limb dystonia, postural instability, and disturbances of language.
  • There is often marked and disabling apraxia of the affected limb, where it becomes difficult or impossible to control the movements of the affected limb even though there is no weakness or sensory loss.
  • No laboratory/brain scan tests exist to confirm the diagnosis of CBD. CBD is a clinical diagnosis.
  • There is no specific treatment for CBD.
  • Supportive treatment such as botulinum toxin (Botox) for dystonia, antidepressants, speech and physical therapy may be helpful.
  • Levodopa and dopamine agonists (common PD medications) seldom help.
     

IV. Multiple System Atrophy (MSA)

  • MSA is a larger term for several disorders in which one or more system in the body deteriorates.
  • Included in the category of MSA are: Shy-Drager syndrome (DSD), Striatonigral degeneration (SND) and OlivoPontoCerebellar Atrophy (OPCA).
  • The mean age of onset is in the mid-50s.
  • Symptoms include: bradykinesia, poor balance, abnormal autonomic function, rigidity, difficulty with coordination, or a combination of these features.
  • Initially, it may be difficult to distinguish MSA from Parkinson’s disease, although more rapid progression, poor response to common PD medications, and development of other symptoms in addition to Parkinsonism, may be a clue to its diagnosis.
  • No laboratory/brain scan testing exists to confirm the diagnosis of MSA.
  • Patients respond poorly to PD medications, and may require higher doses than the typical PD patient for mild to modest benefits.
  •  

V. Vascular Parkinsonism

  • Multiple small strokes can cause Parkinsonism.
  • Patients with this disorder are more likely to present with gait difficulty than tremor, and are more likely to have symptoms that are worse in the lower part of the body.
  • Some will also report the abrupt onset of symptoms or give a history of step-wise deterioration (symptoms get worse, then plateau for a period).
  • Dopamine is tried to improve patients’ mobility although the results are often not as successful. 
  • Vascular Parkinsonism is static (or very slowly progressive) when compared to other neurodegenerative disorders.

Did you know that Dementia with Lewy Bodies is second to Alzheimer’s as the most common cause of dementia in the elderly?

 

VI. Dementia with Lewy bodies (DLB)

  • DLB is a neurodegenerative disorder that results in progressive intellectual and functional deterioration.
  • Patients with DLB usually have early dementia, prominent hallucinations, fluctuations in cognitive status over the day, and Parkinsonism.
  • Cognitive changes in patients with DLB include deficits in attention, executive function (problem solving, planning) and visuospacial function (the ability to produce and recognize figures, drawing or matching figures).
  • There are no known therapies to stop or slow the progression of DLB.

 

 

 

 

 


 

 

 

 
 
 
 
 
 
 
 

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