Mary, in her early 60’s, had been bothered by a tremor in her right hand.  It became gradually more notable.  It had embarrassed her when she had been out to dinner.  It terrified her when it was time to sign her name to a check while in the checkout line at the market.  When she finally saw her primary care physician, she noted that she was more likely to hold her husband’s arm when out walking in public to steady herself.   She had more difficulty getting up and down from sitting. Her family had seen a change in her facial expressions, she seemed less likely to smile and laugh and at times had a blank facial appearance.

Her physician had her see a neurologist, who by exam and evaluation suspected that she had Parkinson’s syndrome.  He suggested beginning a medication- carbidopa-levodopa (trade name Sinemet), to see if it would improve her tremor and other symptoms.  And indeed, things were better.  Her tremors lessened, her movements were more fluid and steady, and even the smile returned to her face.  Her neurologist concluded based on her symptoms and the response to the medications that indeed this was Parkinson’s disease.

Over the next year, Mary found her symptoms and response to the medications were uneven.  She also began to experience bouts of anxiety, especially at periods when the effects of her medication seemed to wane.  She also found herself feeling more sad and depressed.  While she knew it was important to stay active, she found it increasingly difficult to motivate herself to get done the simple tasks and routines of her day. Having a degenerative illness and brain disease was an obvious source of worry and depressed her.

Parkinson’s disease (PD) is a neurodegenerative movement disorder that is the result of the loss of dopamine-producing brain cells.  It is chronic and progressive in course.  It is a syndrome most often characterized by muscle rigidity, tremors, slowing movement, and postural instability. Other symptoms may include depression, anxiety, apathy, difficulty with swallowing, difficulty with speaking, and sleep disruptions.

In its most classic presentation, it is known as primary parkinsonism or idiopathic parkinsonism, in which the disease is not associated with a clear cause; though genetic factors have been discovered.  Primary parkinsonism is what is meant when we use the term “Parkinson’s disease”, named after the English physician who first described the condition in 1817.   However, there are many other causes leading to parkinsonian symptoms, referred to as secondary parkinsonism.  These include head trauma, infectious agents such as viral illness, and commonly toxicity associated with medications that block dopamine transmission such as antipsychotics.  It is estimated that 1 in 300 individuals will develop PD in their life time.  Risk factors for PD include aging, male gender, family history and specific genetic risks, exposure to environmental toxins such as pesticides, head trauma, and low levels of folate.

There is no cure for PD, but there are a variety of different medications that can provide significant symptomatic relief and benefit.  The primary goal of medication therapy is to replace dopamine in the brain.  Carbidopa-levodopa is the gold-standard treatment.  Carbidopa delays the breakdown of the substituted dopamine (levodopa) so that it can effectively get into the brain. There are many other agents the neurologist may use to enhance the effect of carbidopa-levodopa or mimic the action of dopamine itself.  Newer therapies include deep brain stimulation in which electrodes are placed into specific brain regions to help balance and facilitate normal movement and help reduce the need for medications.

While it is difficult to know just how frequently depression complicates PD, it is estimated that nearly 50% of Parkinson’s patient will suffer from depressive symptoms, including anxiety during the course of illness.  Depression and anxiety often appear in the early stages.  It is thought that these symptoms are often under diagnosed and not treated.  We have found that with counseling and support, education around the nature of the illness, expectations of the effects of parkinsons medications, and reassurance around the nature of anxiety and depression as complicating symptoms; patients and families are much better able to cope with the illness.  Depression and anxiety can often be targeted and effectively treated with antidepressant medications and anti-anxiety medications, with significant benefit — improving overall disability and quality of life.

In addition to the management of emotional symptoms, the psychiatrist or neurologist may need to address troubling side-effects related to the primary parkinsons medications themselves.  Medications such as carbidopa-levodopa and other medications designed to improve dopaminergic function may contribute to hallucinations and paranoid thought.  First strategy is to attempt to reduce and find the right balance of medications that benefit the movement symptoms without causing psychiatric symptoms.  Cautious use of select low-potency dopamine blockers may help alleviate psychiatric symptoms, but need to be used judiciously as to not worsen the overall movement symptoms.

In Mary’s case, her anxiety and depressive symptoms improved with counseling, education, and the addition of medication.  She found her days much more active, and social, and she was better able to cope with the challenges she faced with PD.

For more information, the reader is directed to the following resources: American Parkinson Disease Association (adpa@adpaparkinson.org), National Parkinson Foundation (www.parkinson.org), Michael J. Fox Foundation (www.michaeljfox.org) and the National Institute of Neurological Disorders and Stroke (www.ninds.nih.gov/disorders/parkinsons_disease).

by Dr. Michael A. Keys, MD

Dr. Keys is a geriatric psychiatrist, Adjunct Associate Clinical Professor of Psychiatry at the University of Cincinnati College of Medicine, and Director of Senior Services at the Lindner Center of HOPE, Mason, Ohio.