A Brief Review of AFP's "Parkinson Disease: An Update"

This is a synopsis of:

Parkinson Disease: An Update

JOHN D. GAZEWOOD, MD, MSPH, University of Virginia Health System, Charlottesville, Virginia

D. ROXANNE RICHARDS, MD, MedStar Physician Partners at St. Clement's, Leonardtown, Maryland

KARL CLEBAK, MD, Lake Monticello Primary Care, Palmyra, Virginia

Am Fam Physician. 2013 Feb 15;87(4):267-273.

     Parkinson disease is a progressive neurodegenerative disease with symptoms of rigidity, tremor, micrographia  shuffling gait, and postural instability. The symptoms are progressive. The disease is due to degeneration of the dopaminergic neurons in the substantia nigra. There is also lewy body development as well. Although the disease is almost exclusively clinical, a positive response to levodopa can help with the diagnosis. The disease is especially tough to diagnose in the early stages, and there is often a large differential.
     As far as imaging is concerned, it has not helped much with the diagnosis other than single-photon emission CT. This has been shown to distinguish Parkinson disease from essential tremor and non-degenerative Parkinson.
     Treatment can be broken down into early and late therapy. There is a concept of "on time" and "off time" in Parkinson disease. "On time" is when the medicine is working and "off time" is when the symptoms are reoccurring. Early therapy is when there is sufficient "on time", and late therapy is used when "off time" occurs.  In early therapy, levodopa/ carbidopa, non-ergot dopamine agonists,  and MAO-b inhibitors are useful. Levodopa/ carbidopa had been very effective for motor symptoms  but is associated with dyskinesia. Dopamine agonists are less effective for motor symptoms, but associated with a lower incidence of dyskinesia.
     Late therapy should be used when the initial therapy becomes less and less effective. At that point, we can add the dopamine agonists and MAO-b inhibitors to the levo/carbidopa. Catechol O-methyltransferase inhibitors (which slows down levodopa metabolism) should be avoided due to the side effect of hepatotoxicity. Amantadine has been shown to reduce dyskinesia, but only for about 8 months, thus is has limited usefullness
     Deep brain stimulation of the subthalamic nucleus and globus pallidus interna is another option. Patients should be free of comorbidities, depression, cognitive impairment, and have had a good response to levodopa. There are significant side effects too that should be considered, which are detailed in the article.
     Physical and occupational therapy can be very effective in maintaining the patient's quality of life, depending on how advanced the disease is.
     Besides the motor symptoms, there are other issues to address. These other symptoms can also affect the patients quality of life.  Fatigue is  a common problem which can be helped with methylphenidate. Drooling can be treated with Botox or glycopyrrolate. TCA's may help with depression, but you must watch for the anticholinergic side effects. Quetiapine or clozapine can be used for psychosis (clozapine and cause agranulocytosis). Dementia is a major side effect and can be treated with Donepezil (or rivastigmine in some small studies).