Parkinson’s Disease Dementia (PDD)

ConditionsParkinson’s Disease Dementia (PDD)

As the years progress, patients living with Parkinson’s disease may develop cognitive decline, trouble with decision making, personality changes, and short-term memory complaints.

If the cognitive changes result in difficulty with daily functions, such as affecting work or managing medications, this is called dementia due to Parkinson’s disease or Parkinson’s disease dementia (PDD).

It is important to note that PDD is not the same as Alzheimer’s disease (AD). Patients with Parkinson’s disease (PD) are not at risk of developing AD. The cognitive changes of PD, even when severe enough to cause dementia, are not the same as those of AD. Typically long-term memory is not as affected, and patients retain recognition of loved ones and a general sense of awareness.

Cognitive changes and dementia can affect the vast majority of patients with PD, with the risk accumulating as the years pass and with greater age. Unfortunately the Parkinson’s prognosis is that around 75 percent of patients living with PD for more than ten years will develop dementia.

Rather than considering this as an inevitability, our focus at the Pacific Brain Health Center and Pacific Movement Disorders Center is to challenge ourselves and our patients to change the course of PD and find novel ways of preventing dementia.

Signs and symptoms of Parkinson’s disease dementia include:

  • Mental inflexibility (e.g., difficulty adjusting to schedule changes, trouble changing focus)
  • Short-term memory issues and memory loss (which can affect accuracy of taking medications on time)
  • Trouble with decision making
  • Executive function difficulty (e.g., making plans, understanding activities requiring complex steps)
  • Slow processing speed (i.e., the words or answers are there but take longer to come)
  • Inattention (e.g., fleeting thoughts)
  • Visual processing difficulty (e.g., depth perception)

Non-motor symptoms that can be associated with PDD include:

  • Psychosis (i.e., disconnect from reality):
    • Hallucinations (e.g., perceiving children, people, or animals that aren’t there)
    • Delusions (i.e., fixed false beliefs such as paranoia, suspicions of cheating spouses)
  • Agitation
  • Sleep disturbances (e.g., trouble falling asleep, trouble staying asleep, REM sleep behavior disorder)
  • Depression
  • Anxiety

Diagnosis of PDD typically requires the initial diagnosis of PD, with the signs of Parkinson’s disease of rest tremor, bradykinesia (slowness and smallness of movements), rigidity (stiffness), and postural instability.

At Pacific Movement Disorders Center we regularly monitor patients for cognitive changes which could signal the beginning of dementia, utilizing evidence-based screening tests. If concern arises, detailed neuropsychological evaluation with clear delineation of cognitive strengths and weakness can be obtained. On occasion, volumetric MRI scanning or PET scanning may play a role.

Differentiating between PDD and Dementia with Lewy Bodies (DLB) can be challenging, given both conditions pertain to dementia (cognitive decline) and parkinsonism (slowness, stiffness, tremor, imbalance).

Lewy Bodies in PD patients predominate in the deep part of the brain called the substantia nigra, whereas in DLB they are widespread from onset.

The main differentiating factor is the clinical history:

In PDD, parkinsonism comes first, typically years prior to onset of dementia, whereas in DLB, cognitive changes either precede or coincide with onset of parkinsonism.
In PDD, there tends to be clear improvement with levodopa for the motor symptoms at least.

For more on differentiating between PDD and DLB, see this comparison table.

It may be noted that patients with PD (with or without dementia) may have episodes of confusion or disorientation in the context of delirium, which can be precipitated by toxins, medications, or infections. Delirium waxes and wanes, so sudden declines in orientation, language, and behavior should prompt evaluation such as laboratory work, urinalysis, and potentially chest X-ray and MRI. It is important to reassure family members witnessing abrupt declines that patients are likely to recover to baseline after the underlying cause is managed.

Currently, statistics on cognitive change and dementia in PD come from studying patients who were first diagnosed ten or twenty years ago, prior to widespread recommendations about physical activity and exercise.

While no treatments have been proven to prevent development of Parkinson’s and dementia, there is strong reason to believe that physical and cognitive activity could play a powerful role in slowing disease progression in the early stages of Parkinson’s disease and throughout the course of disease.

Treatment of PDD involves the use of rivastigmine, an oral or transdermal (patch) medication that boosts the brain’s acetylcholine (one of the key neurotransmitters or brain chemicals).

Rivastigmine (Exelon) is the only medication FDA approved for PDD but other medications sometimes used “off label” include donepezil (Aricept), also an acetyhlcholine boosting drug, and memantine (Namenda), an NMDA receptor antagonist.

Medications for dementia help somewhat, and other treatments may play a role for behavior issues in PDD.

Research, including clinical trials, is ongoing to find disease-modifying treatments for PDD.