Uncovering the Mystical Treatment of Deep Brain Stimulation

Authored by: Noah Goodman

Art by: Andrew Mo

According to recent estimates, there are more than 1 million Parkinson’s patients in the United States, and over 90,000 new diagnoses are made each year [1]. Furthermore, Parkinson’s disease can permeate nearly all aspects of a person’s life. For example, many Parkinson’s patients experience muscle tremors – leading to poor motor control – and atypical (e.g. slurred, soft, and muffled) speech – leading to difficulties communicating with friends and family [2]. Furthermore, many patients experience psychosocial and psychophysical comorbidities, such as anxiety and sensory deficiencies, respectively [2]. Moreover, in a study including almost 50,000 participants, researchers found that ten-year mortality rates (i.e. the chance of dying in the next ten years) were more than twice as high amongst Parkinson’s patients compared to match (i.e. same age and same sex) control participants, with the leading cause of death amongst Parkinson’s patients being nervous system disease [3]. Thus, there is a serious need for effective treatments and interventions geared at reducing the symptoms and progression of Parkinson’s Disease. But how could such a pervasive disease be treated?

Parkinson’s Disease is characterized (at least within the scope of this article) by a loss of dopamine-producing neurons in the midbrain [4]. While the exact mechanism may be more complex than described here, it is sufficient to consider dopamine to be a neurotransmitter involved in directing motor movements, and therefore, the lack of dopamine production in the midbrain yields motor irregularities. Dopamine also plays a critical role as the chemical messenger of the mesolimbocortical system, which modulates reward preferences and is likely heavily involved in mood regulation [5]. This provides a mechanistic basis for the psychological impacts of Parkinson’s Disease. 

Given that Parkinson’s patients seem to suffer from dopamine insufficiencies, it is no surprise that the most common treatment is Carbidopa-levodopa (e.g. Sinemet), with levodopa being a chemical that is converted to dopamine upon reaching the brain, and carbidopa being a chemical that helps the levodopa reach its target cells [6]. While the drug is quite effective, many patients experience unpleasant side effects, ranging from nausea and fatigue to dyskinesias and hallucinations [7]. Thus, alternative interventions would be beneficial in order to treat patients who either (1) cannot tolerate levodopa, (2) experience unpleasant side effects from the drug, or (3) do not show drug-attributed improvements in their condition, symptoms, or progression. 

One exciting alternative intervention for Parkinson’s Disease is known as Deep Brain Stimulation (DBS). DBS involves a surgeon placing thin metal wires in the brain which send electrical impulses through target neurons to control motor movements [8]. While the exact mechanistic details of DBS are still being debated, the procedure has shown great promise as an effective Parkinson’s intervention. For example, Benabid (2003) provided evidence to support the claim that DBS may be as effective as levodopa in improving Parkinson’s-related muscle tremors, while avoiding many of the drug’s disadvantageous side effects [9]. 

Mechanistically, Benadbid (2003) claimed that DBS disrupts the abnormal neural messages associated with Parkinson’s disease, thereby mimicking levodopa’s net effect on the brain [9]. Furthermore, according to Volkman (2004), DBS increases neural metabolism and cerebral blood flow, thereby improving synaptic functioning [10]. Shockingly, Alam et. al (2025) recently provided strong evidence supporting the notion that DBS may even be an effective intervention for treating Alzheimer’s Disease (which has been thought to involve generalized plaque build-up in the brain, rather than targeted death of dopamine neurons), suggesting that Alzheimer’s Disease’s mechanistic properties may be even more complex than previous research had suggested [11]. 

While the mechanism of DBS is somewhat unclear, results of clinical trials seem to support its impressive efficacy [8, 11]. But where can we go from here? 

I believe that the parallel development of sensitive fMRI analysis tools may provide an opportunity to improve upon current DBS procedures. Neuropsychological researchers should aim to localize subregions of the mesencephalon which seem to be responsible for Parkinson’s symptoms. Specifically, studies should be run that correlate functional deficiencies in the Parkinson’s-affected brain with specific symptoms. Thus, different Parkinson’s patients who present different symptoms may receive DBS interventions that specifically target their area of deficiency and thereby (presumably) yield more consistent improvements in clinical condition. While fMRI does not have the resolution to track dopamine signaling per se, I do not think that such an ability is necessary or even particularly constructive. fMRI will track macroscopic (activational, as operationalized by Blood Oxygen Level Dependent contrasts) deficiencies in brain functioning due to Parkinson’s disease, which is what DBS aims to treat. Thus, I believe that fMRI-based research on Parkinson’s patients is an important future avenue for improving DBS treatments. 

While Parkinson’s Disease is an increasingly prevalent neurodegenerative disorder in the United States, recent improvements in interventional treatments such as DBS and research techniques, such as fMRI, provide a reason for optimism, as together, they provide a very promising treatment avenue. 

References

1. Statistics. (2026). Parkinson’s Foundation. https://www.parkinson.org/understanding-parkinsons/statistics 

2. Mayo Foundation for Medical Education and Research. (2024a). Parkinson’s disease. https://www.mayoclinic.org/diseases-conditions/parkinsons-disease/symptoms-causes/syc-20376055 

3. Ryu, D. W., Han, K., & Cho, A. H. (2023). Mortality and causes of death in patients with Parkinson's disease: a nationwide population-based cohort study. Frontiers in Neurology, 14, 1236296.

4. Ramesh, S., & Arachchige, A. S. P. M. (2023). Depletion of dopamine in Parkinson's disease and relevant therapeutic options: A review of the literature. AIMS neuroscience, 10(3), 200.

5. Serafini, R. A., Pryce, K. D., & Zachariou, V. (2020). The mesolimbic dopamine system in chronic pain and associated affective comorbidities. Biological psychiatry, 87(1), 64-73.

6. Mayo Foundation for Medical Education and Research. (2024b). Parkinson’s disease. https://www.mayoclinic.org/diseases-conditions/parkinsons-disease/diagnosis-treatment/drc-20376062 

7. Rebecca Gilbert, M. (2024). Carbidopa/levodopa: Side effects, dosages, & faqs: APDA. American Parkinson Disease Association. https://www.apdaparkinson.org/article/common-questions-about-carbidopa-levodopa/ 

8. Deep Brain stimulation. (2026). The Michael J. Fox Foundation for Parkinson’s Research. Parkinson’s Disease. https://www.michaeljfox.org/deep-brain-stimulation 

9. Benabid, A. L. (2003). Deep brain stimulation for Parkinson’s disease. Current opinion in neurobiology, 13(6), 696-706.

10. Volkmann, J. (2004). Deep brain stimulation for the treatment of Parkinson’s disease. Journal of clinical neurophysiology, 21(1), 6-17.

11. Alam, J., Bhattacharjee, S., Chakraborty, S., Rahman, S. Z., Hasan, A., Haseen, M. A., & Sarfraz, M. (2025). Neuromodulation via brain stimulation: A promising therapeutic perspective for Alzheimer's disease. In Artificial Intelligence in Biomedical and Modern Healthcare Informatics (pp. 257-266). Academic Press.