Parkinson's Nurse Navigator
A Newsletter for Nurses in Neurology
In This Issue
Quick Links
Join the Navigator
Email List

Join Our Mailing List
Archived Issues:

1st Quarter
2nd Quarter

3rd Quarter

Issue: #4 December/2010
Nurse Navigator

The Nurse Navigator is a quarterly e-newsletter focusing on best practices in nursing care for patients with Parkinson's and other related movement disorders. Articles will be written by nurses, mid-levels and specialists with a wide range of experience and expertise.

Since many patients rely on nursing care as their primary contact and information source we thought it would be helpful to provide information, tools and insights from fellow practitioners.

If you know of other colleagues that would benefit from this newsletter, please do forward it along.

Thanks for reading.


Colleen Crowley
877-980-7500 |

Parkinson's - More than just a movement disorder 

Cognitive and behavioral problems are significant challenges in the treatment of Parkinson's disease.

Parkinson's disease (PD) is a movement disorder characterized by tremor, rigidity, bradykinesia and postural instability.   Focus on these easily identified motor signs often overshadows the many nonmotor symptoms that coexist in this disorder. Under recognition of nonmotor symptoms by clinicians may reflect the tendency to focus primarily on the more apparent motor features of PD and/or lack of awareness of the nonmotor symptoms. Depression and cognitive problems are considerable concerns given the direct impact they have on QOL. In fact these problems contribute significantly to impair QOL and their effect together is synergistic- affecting lives more significantly than motor function.

Cognitive issues in Parkinson's 

Hallucinations and REM sleep disorder can be associated with or a  precursor to cognitive difficulties such as dementia .

"My patient's wife complains that her husband has vivid dreams and often awakens confused. Is this related to Parkinson's disease?"

Nurses are in a unique position to identify certain symptoms often brought forth by the carepartner. Certain symptoms place patients at an increased risk for future cognitive or behavioral problems the impact of which can be minimized.


Caregivers often confuse vivid, physically active dreams with nighttime hallucinations and certainly both can be present.  Hallucinations are usually visual in nature and can range from fleeting illusions of simple shapes in peripheral vision to well formed objects such as people or animals.  Sight is sometimes maintained early in the disease but can be lacking in more severe cases leading to significant distress.

REM sleep behavior disorder (RSD) is a condition described as a very vivid, intense, frightening, physical and often unpleasant dreams and the presence of vivid dreams may be a precursor to psychosis and dementia (Hickey 2007).  Bed partners may describe the patient physically 'acting out' their dreams- punching, kicking and yelling.  The symptoms of RSD can precede PD motor symptoms and its presence may increase future risk of dementia. Reducing medication (as described in hallucination treatment below) can help restless nights including RSD. Clonazepam is an effective treatment for RBD and should be considered if sleep is disrupted or patient safety becomes a concern.

Cognitive problems and high levels of dopaminergic medicines increase the risk of developing visual hallucinations.  In general, selegiline, amantadine, and dopaminergic agonists are associated with a higher risk of hallucinations than levodopa.  If visual hallucinations are present early in the course of the disease and are accompanied by loss of sight and cognitive fluctuations, a consideration of Lewy Body Dementia (LBD) may be warranted (McKeith 2006). LBD is characterized by parkinsonian symptoms and early onset visual hallucinations, fluctuating level of consciousness, and neuroleptic sensitivity.

Monitoring and treatment of psychosis is paramount as it is a major risk factor for nursing home placement[53]. Treating hallucinations requires a multi-tiered approach.  The stepwise approach to treat psychosis in patients with PD should involve (1) a search for systemic illness such as urinary tract infection, aspiration pneumonia, dehydration or other co- morbid problem, (2) reduction of CNS active medications (i.e. narcotics, bladder antispasmodics), and (3) if possible, reduction of anti-PD medications with greatest cognitive side effect risk.  In many cases, the latter is not a realistic option and addition of an antipsychotic may be necessary.

Conventional neuroleptics (i.e. haloperidol) should be avoided since their dopamine blocking affect can worsen parkinsonian motor symptoms. Certain atypical neuroleptics appear to be the best tolerated in PD patients. Clozapine is the only neuroleptic found to be more efficacious than placebo in patients with PD.  However, the higher risk of side effects and frequent blood monitoring make its use difficult. Early studies suggested that quetiapine is equally effective but a recent controlled study failed to show efficacy.  Quetiapine is considered the first-line treatment option given its better safety profile (Miyaski, 2006). Other atypical antipsychotics appear to exacerbate PD or have not been adequately studied and should therefore be used with extreme caution.

Clinical pearl: Ask about the presence of hallucinations. Many patients do not volunteer this problem during history yet the presence greatly affects future treatment decisions. Search for causes other than Parkinson's if there is an acute exacerbation such as medicine change, dehydration, injection or other systemic illness.  

Dementia in Parkinson's 

Unlike Alzheimer's disease, memory problems are not the initial complaint in Parkinson's dementia.


Dementia can occur in about 20-30% of patients with Parkinson disease (Aarsland, 2005).  Parkinson's dementia is one of the classic sub-cortical dementias and differs from Alzheimer's disease and other cortical dementias associated with problems such as memory loss, language difficulties or apraxia. The cognitive problems in PD represent a continuum ranging from mild cognitive deficits to dementia.


Risk factors for development of dementia include age, lower education, male gender, presence of hallucinations, depression, sleep disturbance, and disease duration (Galvin, 2006).

Treatment requires attention to hallucinations if present, reduction in any cognitive impairing medicines and direct cognitive therapy. The acetylcholinesterase inhibitor, rivastigmine, can improve cognitive function, hallucinations and apathy (Emre, 2004).

Optimal treatment of dementia requires a multidisciplinary approach.  Although vigorous research is not yet available, there is growing evidence that exercise, music and dance therapy, art, and social engagement and human touch are helpful.

Clinical Pearl: use visual and verbal ques to combat memory problems. Keep tasks simple, focusing on just one step at a time.  Avoid overstimulation and multitasking.




Depression as a sympton of disease 

Depression, like other cognitive behavioral symptoms, is both under-recognized and undertreated.

Depression is among the most common neuropsychiatric symptoms in PD with a prevalence of up to 76% of patients with PD ( Veazey, 2005). The diagnosis of depression in PD is critical due to its impact on physical symptoms, cognitive status, perception of quality of life, and caregiver distress.  Depression can be difficult to diagnose.  Loss of spontaneous facial expression, bradyphrenia, apathy, and social withdrawal due to apathy or physical disability can be mistaken for depression.  The Beck Depression Inventory is sensitive to the depression evident in PD and thus, may be a reasonable tool to screen patients for depression.

Depression can occur as a general feature but also as an end of dose phenomenon emerging just prior to the patient's next dose of levodopa.  It is important to ask patients if their depression fluctuates throughout the day to assess the possible relationship to dopaminergic therapies.  Depression can also coexist with anxiety.

Psychotherapy and behavioral techniques such as cognitive behavioral therapy and guided relaxation, attention to sleep hygiene, social engagement and exercise are first line therapies for mild depression.  Medical therapies include SSRIs especially when anxiety is a problem and nonselective agents.  All serotonergic agents should be used with caution in combination with MAO inhibitors, which are often employed for the treatment of motor symptoms in PD, due to the risk of developing serotonin syndrome.  Serotonin syndrome is characterized by fever, altered mental status, myoclonus, tremor, hyper-reflexia, and diaphoresis and may be fatal.

Apathy is present in approximately 30% of patients with PD (Kirsch-Darrow, 2006). Apathy can occur with depression and without depression.  The diagnosis of apathy without depression should be considered if no improvement is noted with standard therapy.

Clinical pearl: Apathy is poorly treated with medicines but can respond to a behavioral approach.  When apathy is severe, it can significantly limit daily ADLS. An occupational therapist or recreational therapist can help you establish a schedule, prioritize activities and set a strategy to accomplish important tasks.



Dr. Monique Giroux is the medical director of the Northwest Parkinson's Foundation. She specializes in movement disorders with a focus on rehabilitation and wellness for Parkinson's patients.


Aarsland, D., J. Zaccai, and C. Brayne, A systematic review of prevalence studies of dementia in Parkinson's disease. Mov Disord, 2005. 20(10)(Oct): p. 1255-63.


Emre, M., et al., Rivastigmine for dementia associated with Parkinson's disease. New England Journal of Medicine, 2004. 351: p. 2509-2518.


Galvin JE, Pollack J, Morris JC. Clinical phenotype of Parkinson disease dementia. Neurology. Nov 14 2006;67(9):1605-11.

Hickey, M., et al., "Idiopathic" rapid-eye-movement (REM) sleep behavior disorder is associated with future development of neurodegenerative diseases. Neurologist, 2007. 13(2): p. 98-101.

Kirsch-Darrow, L., et al., Dissociating apathy and depression in Parkinson disease. Neurology, 2006. 67(1)(Jul 11): p. 33-8.

McKeith, I. , Consensus guidelines for the clinical and pathologic diagnosis of dementia with Lewy bodies (DLB): report of the Consortium on DLB International Workshop. J Alzheimers Dis, 2006. 9(3 Suppl): p. 417-23.

Miyasaki, J., et al., Practice Parameter:  Evaluation and treatment of depression, psychosis, and dementia in Parkinson's disease (an evidence based review).  Report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology, 2006. 66: p. 996-1002.

Connie Veazey, Ph.D., Sahinde Ozlem Erden Aki, M.D., Karon F. Cook, Ph.D., Eugene C. Lai, M.D., Ph.D. and Mark E. Kunik, M.D., MPH. Prevalence and Treatment of Depression in Parkinson's Disease .  J Neuropsychiatry Clin Neurosci. 2005. 17:310-323.

NWPF logo

The Northwest Parkinson's Foundation (NWPF) plays a vital role in helping people with Parkinson's live meaningfully with the disease. A large part of our mission is education, both for the medical professional and for patients, caregivers and families. At both levels we have the opportunity to improve the day-to-day for those touched by this debilitating disease set. With the addition of Dr. Monique Giroux as Medical Director, we have become a recognized leader in professional education as well as patient education.


The NWPF currently serves 25,000 people throughout the Northwest and beyond. Our primary constituency resides in the Northwest (Washington, Oregon, Idaho, Montana and Alaska), home of 70,000+ Parkinson's patients.

This program is generously supported by educational grants from Teva Neuroscience.