PHARMACOLOGIC TREATMENT OF PARKINSON’S DISEASE
characterized by motor and non-motor symptoms1,3,4,6. This study is about spreading what is known about
the therapeutic approach in order to promote the best treatment. Objective: To present the
pharmacologic treatment to PD highlighting its benefits and risks. Materials and Methods: This literature
review used books and articles published in English and Portuguese in the databases of “Medline”,
“Scielo” and “PubMed”. Results: To select the articles for this study, the keywords used were “Parkinson”,
“treatment” and “pharmacological”. The articles selected were among the most relevant with free text
available. Discussion and Conclusion: The goal of the drug treatment is to increase levels of dopamine
and reduce the action of acetylcholine2. Levodopa has been the most important drug in the symptomatic
treatment of PD improving motor manifestations, promoting independence and quality of life1,3,6. Nausea,
vomiting and orthostatic hypotension are the most common acute side effects caused by the peripheral
action of dopamine. Dyskinesias are important side effects related to plasmatic concentration of the drug
and they worsen with the progression of the disease. Also may occur falls, freezing of gait, autonomous
dysfunction, sleep disorders and impaired cognitive function1,3,6. In long-term treatment the effect of the
drug wears-off and so does its benefits1,3,4,6. Options for the treatment of PD are a) Dopamine agonists
act on the dopaminergic receptors and may be useful in the initial treatment. Compared to levodopa they
have longer action and lower risks of dyskinesias, although they’ve showed more risks for hallucinations,
cognitive dysfunction and disorders related to control of impulse1,3; b) MAO-B inhibitors block the central
metabolism of dopamine, therefore increasing its levels on the synapses and reducing oxidative stress.
They possess little benefit on the parkinsonism and may enhance dyskinesias if associated with
levodopa1,3. It’s believed that MAO-B inhibitors have neuroprotection effects because studies in animal
models showed decrease of neurodegeneration and retardation of the disease’s progression7,8; c) COMT
inhibitors increase levodopa’s half-life and bio-availability. Side effects include nausea, vomiting and
increase of dyskinesias1,3 ;d) Centrally active anticholinergic agents have limited use in the elderly for their
side effects as urinary dysfunction, glaucoma and cognitive impairment1,3; e) Dopamine precursors and
peripheral DOPA-descarboxylase inhibitors enhance effects of levodopa allowing a reduction of dose and
maintaining equivalent benefit. Besides, they block the formation of peripheral dopamine that acts on the
vomiting center, reducing nausea9; f) Dopamine releasing agents increase the release and block the
uptake of dopamine by synaptic terminals and have action on motor symptoms9; g) Peripheral
antidopaminergic agents don’t penetrate the CNS barrier and they’re used to avoid nausea of levodopa
and dopamine agonists9; h) Antidepressants, anxiolytics and antipsychotics are used to treat associated
neuropsychiatric symptoms9. There’s no consensus about how to treat Parkinson’s Disease, so it’s up to the physician to manage each case. Therefore, it’s required knowledge of the therapeutic arsenal available
since PD is a chronic and progressive disorder that affects millions of people in the world.
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