Treating Parkinson’s disease

Click here to read about the common therapeutic strategies used to manage the progression of Parkinson’s disease.
Last update10th Feb 2023

The principal medication used to manage Parkinson’s disease (PD) is levodopa, which is commonly known as L-Dopa. Experts believe that L-Dopa may have a limited period of efficacy, so many specialists try to avoid its use early in the disease’s progression. However, this is not proven and should simply be a management consideration.

Other medications such as monoamine oxidase type B (MAO-B) inhibitors, selegiline, rasagiline, dopamine agonists, and amantadine seem to offer some symptomatic relief, so they can be administered initially. Anticholinergic medications are sometimes used when tremor is a prominent symptom.

Figure 1. Medications commonly used to manage Parkinson’s disease include levodopa (L-Dopa), monoamine oxidase type B (MAO-B) inhibitors, selegiline, rasagiline, dopamine agonists, amantadine, and anticholinergics.

Treating PD with L-Dopa and carbidopa

Unfortunately, both the motor and non-motor components of the disease do progress, and most patients are eventually started on L-Dopa. Levodopa is a chemical that is converted to dopamine in the brain. Often, L-Dopa is combined with a dopamine decarboxylase inhibitor called carbidopa.

L-Dopa is still the most effective medical treatment, controlling the most bothersome PD symptoms. Initially the improvement can be quite dramatic, even with low doses.

Figure 2. The combination of levodopa and carbidopa is commonly used in patients with Parkinson’s disease and is considered the gold standard treatment.

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Carbidopa reduces the systemic adverse effects of L-Dopa, which can include hypotension, dysrhythmia, decreased kidney function, and gastrointestinal distress. The combination of L-Dopa and carbidopa is considered the gold standard treatment of PD.

While treatment with levodopa and carbidopa reduces many of the motor symptoms of PD, it doesn't seem to help with progressive cognitive loss or depression. These symptoms are common non-motor components of PD as it progresses.

Figure 3. The medications levodopa and carbidopa are effective at reducing motor symptoms in patients with Parkinson’s disease (PD). But, they do not help with the symptoms of cognitive loss and depression, which are commonly associated with PD.

The daily duration for which levodopa and carbidopa treatment remains effective typically diminishes over time. In other words, patients experience shorter periods of good function (on periods) and longer periods of PD symptoms (off periods). As a result, dosages are invariably increased and patients experience more motor side effects—principally dyskinesias that are often choreiform in nature.

Additional medications that can be added to a PD treatment regimen

There are four strategies you may want to consider if your patient is experiencing a shortened duration of effectiveness with levodopa and carbidopa treatments:

  1. Adding a dopamine agonist or a MAO-B inhibitor to the regimen
  2. Increasing the frequency of levodopa / carbidopa dosages
  3. Adding a between-dose inhaled levodopa
  4. Switching to sustained-release forms of levodopa and carbidopa
Figure 4. The four strategies that can be employed if your patient is experiencing a shortened duration of effectiveness for levodopa and carbidopa include adding a dopamine agonist or monoamine oxidase type B (MAO-B) inhibitors, increasing the frequency of levodopa (L-Dopa) and carbidopa, adding between-dose inhaled L-Dopa, and switching to sustained-release L-Dopa and carbidopa.

In addition to L-Dopa, there is a slew of other medications that are often added for difficult cases of PD. For example, medications to treat depression, sleep disorders, and dementia are commonly prescribed.

Depression is very common in patients with PD, and is likely a due to a mix of neurochemical and situational causes. For a patient with depression, consider employing selective serotonin reuptake inhibitors (SSRIs).

Sleep disorders are also very common, so work to optimize your patient’s sleep hygiene and consider a low dose of benzodiazepines in refractory cases.

As well, dementia is progressive in many patients with PD, and consideration should be given to the employment of cholinesterase inhibitors (such as rivastigmine and donepezil).

Figure 5. Other medications that can be added to the regimen in difficult PD cases includes antidepressants for depression, benzodiazepines for sleep disorders, and cholinesterase inhibitors for dementia.

Other neuropsychological problems such as anxiety, hallucinations, and impulsive behaviors may accompany PD. These may require management with both further pharmaceutical treatment and input from a mental health care professional.

Figure 6. Other neuropsychological problems experienced by patients with PD may require treatment with medication and input from a mental health care professional.

Factors that may affect PD prognosis

Patients may ask you about special diets for microbiome manipulation and the use of neuroprotectant medications; to date, none of these have shown tremendous efficacy. Currently, a common-sense diet is generally recommended featuring grains, nuts, berries, and avoiding foods high in saturated fat, sugar, sodium, and dairy.

Interestingly, cigarette smoking, coffee consumption, and use of nonsteroidal anti-inflammatory drugs (NSAIDs) have been associated with a decreased incidence of PD in the general population. However, the detrimental effects of cigarette smoking offsets any theoretical protective effects that they may have.

High-intensity exercise for PD

A non-medical adjunct to PD therapy, particularly early- and mid-stage PD, has gained much popularity. High-intensity physical workout regimens (often employed with the help of physical therapists) may reduce symptoms for 12 to 24 hours post-workout. These regimens may also improve balance, improve confidence, lower anxiety, and help with situational depression.

Figure 7. High-intensity physical workout regimens may reduce PD symptoms for 12 to 24 hours post-workout.

That’s it for now. If you want to improve your understanding of key concepts in medicine, and improve your clinical skills, make sure to register for a free trial account, which will give you access to free videos and downloads. We’ll help you make the right decisions for yourself and your patients.

Recommended reading

  • Ebersbach, G, Ebersbach, A, Edler, D, et al. 2010. Comparing exercise in Parkinson’s disease—the Berlin LSVT® BIG study. Mov Disord25: 1902–1908. PMID: 20669294
  • Fahn, S, Elton, R, Members of the UPDRS Development Committee. 1987. Unified Parkinson’s disease rating scale. Medscape
  • Hauser, RA, Lyons, KE, McClain, TA, et al. 2020. Parkinson disease. Medscape
  • Huang, A. Cognitive screening toolkit.
  • Kalia, SK, Sankar, T, and Andres, LM. 2013. Deep brain stimulation for Parkinson’s disease and other movement disorders. Curr Opin Neurol26: 374–380. PMID: 23817213
  • Louis, ED, Mayer, SA, and Rowland, LP. 2015. Merritt’s Neurology. 13th edition. Philadelphia: Wolters Kluwer.
  • Uyar, GӦ and Yildiran, H. 2019. A nutritional approach to microbiota in Parkinson’s disease. Biosci Microbiota Food Health38: 115–127. PMID: 31763115

About the author

Gary R. Simonds, MD MHCDS FAANS
Gary is a professor at Virginia Tech Carilion School of Neuroscience and Virginia Tech Carilion School of Medicine.
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