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Medical Author:

Charles Patrick Davis, MD, PhD

Charles Patrick Davis, MD, PhD

Dr. Charles "Pat" Davis, MD, PhD, is a board certified Emergency Medicine doctor who currently practices as a consultant and staff member for hospitals. He has a PhD in Microbiology (UT at Austin), and the MD (Univ. Texas Medical Branch, Galveston). He is a Clinical Professor (retired) in the Division of Emergency Medicine, UT Health Science Center at San Antonio, and has been the Chief of Emergency Medicine at UT Medical Branch and at UTHSCSA with over 250 publications.

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Medical Editor:

Melissa Conrad Stöppler, MD, Chief Medical Editor

Melissa Conrad Stöppler, MD, Chief Medical Editor

Melissa Conrad Stöppler, MD, is a U.S. board-certified Anatomic Pathologist with subspecialty training in the fields of Experimental and Molecular Pathology. Dr. Stöppler's educational background includes a BA with Highest Distinction from the University of Virginia and an MD from the University of North Carolina. She completed residency training in Anatomic Pathology at Georgetown University followed by subspecialty fellowship training in molecular diagnostics and experimental pathology.

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• Some patients' treatment will include or begin with medications (called neuroprotective agents) to "protect" the neurons that make dopamine. Although "neuroprotective agents" protect cells in tissue cultures, it is not clear if they have the same effect on patients' neurons. These medications are monoamine oxidase B inhibitors (MAO-B).
• When patients are given selegiline or rasagiline alone in early PD, it is with the hope that the rate of degeneration of dopamine neurons and/or the breakdown of dopamine in the brain may be slowed.
• Symptomatic therapy is begun when patients have functional disability. The selection of medication depends in part on the nature and cause of the disability. Currently, with a strong presumptive diagnosis of PD, the most effective medication is carbidopa-levodopa; another option sometimes used is levodopa plus benserazide. If a patient's disability is due to bradykinesia, rigidity, decreased dexterity, slow speech, or shuffling gait, they have dopamine-responsive symptoms.
• Patients will be given a medication, such as carbidopa-levodopa (for example, Sinemet) that will increase the dopamine in the brain.
• These medications are started at a low dose, slowly escalated, and adjusted to control symptoms.
• Most people require this kind of treatment for bradykinesia and rigidity within 1 to 2 years after PD diagnosis; many will be started immediately on carbidopa-levodopa.
• An MAO-B inhibitor medication is sometimes added to carbidopa-levodopa treatments.
• If a patient's disability is due solely to tremor, a medication specific for tremors, such as amantadine (Symadine, Symmetrel), an anticholinergic agent, may be used.
• This type of medication provides good tremor relief in about 50% of people but does not improve bradykinesia or rigidity.
• Because tremor may respond to one anticholinergic medication and not another, the doctor may try a second anticholinergic if the first is not successful.

Occasionally, some doctors may prescribe amantadine for short-term treatment of early PD symptoms or use the medication in conjunction with carbidopa-levodopa treatment.

Patients usually will be given medications at the lowest effective dose. Over time, the various medication effects often diminish. To minimize medication side effects, (for example, side effects of memory difficulties, confusion, and hallucinations) the doctor may slowly increase dosages. Side effects involving problems with thinking are relatively common in older patients.

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