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Senevirathne, D.K.L.; Mahboob, A.; Zhai, K.; Paul, P.; Kammen, A.; Lee, D.J.; Yousef, M.S.; Chaari, A. Deep Brain Stimulation. Encyclopedia. Available online: https://encyclopedia.pub/entry/45550 (accessed on 24 June 2024).
Senevirathne DKL, Mahboob A, Zhai K, Paul P, Kammen A, Lee DJ, et al. Deep Brain Stimulation. Encyclopedia. Available at: https://encyclopedia.pub/entry/45550. Accessed June 24, 2024.
Senevirathne, Degiri Kalana Lasanga, Anns Mahboob, Kevin Zhai, Pradipta Paul, Alexandra Kammen, Darrin Jason Lee, Mohammad S. Yousef, Ali Chaari. "Deep Brain Stimulation" Encyclopedia, https://encyclopedia.pub/entry/45550 (accessed June 24, 2024).
Senevirathne, D.K.L., Mahboob, A., Zhai, K., Paul, P., Kammen, A., Lee, D.J., Yousef, M.S., & Chaari, A. (2023, June 14). Deep Brain Stimulation. In Encyclopedia. https://encyclopedia.pub/entry/45550
Senevirathne, Degiri Kalana Lasanga, et al. "Deep Brain Stimulation." Encyclopedia. Web. 14 June, 2023.
Deep Brain Stimulation
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Deep brain stimulation (DBS) is an invasive but established neurosurgical procedure that involves the implantation of one or more electrodes into a targeted brain area, an implantable pulse generator (IPG), and an extension connecting the electrode to the IPG. The IPG contains the battery and circuitry, which generate the electrical signal that is delivered to the targeted brain structure. The DBS system allows for the delivery of electrical pulses to specific areas of the brain with minimal effects on nearby regions.

neurosurgery neurology geriatrics

1. History of DBS

Deep brain stimulation (DBS) is a relatively novel procedure, with most of the research conducted in the past 20 years. Prior to its development, surgical solutions were limited to ablation and the removal of affected brain regions, collectively known as craniotomy [1]. An example of such a procedure is thalamotomy, which entails the excision of the thalamus from the brain or sections of it [2]. While these procedures alleviated bradykinesia (slowness of movement) and dyskinesia (erratic excessive movement), they had major drawbacks including aphasia and dysphagia [3]. Even with the development of more precise surgical procedures such as stereo lesioning [4], the potential for adverse effects from the removal of brain tissue underscores the need for less invasive, better-tolerated therapies.
The use of DBS dates back to 1964, when Ohye et al. used a stereotactic procedure to stimulate the ventrolateral thalamic nucleus [5]. Since then, the volume of research on DBS has steadily increased (Figure 1). Initially, DBS was intended to treat PD and other movement disorders, and the FDA approved its use for PD and essential tremor in 1997 [6]. However, funding for DBS research declined following the development of levodopa in 1969, which may explain the lack of interest until the late 1990s [3]. The approval of thalamic DBS for the treatment of Parkinsonian symptoms in 1997 reignited interest in the field, and the potential applications of DBS in the treatment of other conditions such as AD, dystonia, epilepsy, and psychiatric disorders are currently being heavily researched [3]. As evident in Figure 1, while a significant amount of research has been conducted on the effectiveness of DBS treatment in PD, AD has received far less attention (Figure 1). Thus, further research on the potential use of DBS in AD is necessary.
Figure 1. A graph of the number of research articles published on deep brain stimulation between 1980 and 2022. The queries performed were “DBS and deep brain stimulation”, “DBS and deep brain stimulation and AD and Alzheimer’s Disease”, and “DBS and deep brain stimulation and PD and Parkinson’s Disease”. Search parameters where limited to articles, books, and book chapters. Data extracted from Scopus: https://www.scopus.com (Accessed on 15 December 2022).

2. Current Treatment Plans

DBS can be used to modulate almost all regions of the brain for numerous neurologic conditions. The treatment process begins with the implantation of wires that taper into electrodes in the brain using a precise stereo lesioning procedure [4][7]. Different brain regions can be stimulated to alleviate the effects of different conditions (Table 1).
Table 1. A selection of conditions in which DBS is being actively researched as a viable treatment option.
Once the electrodes are positioned into the desired area of the brain, a separate implantable pulse generator (IPG) device is implanted in the chest wall with leads running under the skin [7]. The IPG can be adjusted externally to deliver a range of frequencies, pulse widths, and amplitudes to the targeted brain region unilaterally and bilaterally [3]. Different frequencies have been used to target specific symptoms, with high frequency stimulation (HFS) defined as above 100 Hz and low frequency stimulation (LFS) as 60–80 Hz [41][42][43]. However, this is quite subjective to each disease, as some papers cite that the range of 10–70 Hz is generally avoided due to the risk of eliciting seizures for epilepsy studies [43]. Some studies have found that frequencies around 60 Hz have restorative effects on PD symptoms, such as reducing aspiration and improving gait [9][44]. In particular, it is noted by di Blaise et al. that HFS systems decrease the levodopa-responsive PD symptoms, whereas LFS systems decrease more axial symptoms of the disease [42]. Indeed, Ramdhani et al. found that PD patients who experienced worsening of their symptoms after receiving HFS DBS had improvements in freezing of gait and dyskinesia when they were switched to a 60 Hz LFS system [44]. Contrastingly, Wyckhuys et al. discovered that HFS systems of 130 Hz are more effective at increasing the threshold and latency of after-discharges in kindled rats, a common animal model of epilepsy [43]. These studies suggest that the use of HFS and LFS systems is dependent on the type of disease that is to be treated, as well as the specific symptoms to be alleviated.

3. Patient Screening

Given the wide range of neurological disorders that can be treated by DBS, it is important to carefully select candidates for the treatment. One important factor to consider is the length of time since the patient’s diagnosis. There is conflicting evidence whether DBS is more effective for patients who were diagnosed within the past 5 years or for those who were diagnosed earlier. For PD, some studies suggest that earlier treatment may be more beneficial [45], while others suggest that it is important to monitor patients over a longer period of time to identify atypical symptoms and assess treatment suitability [46]. Moreover, surgically invasive procedures are usually left as a last-resort treatment and thus are usually used on older patients who have been diagnosed for longer. However, this approach benefits from the ability to rule out other “Parkinson-plus” diseases which may not be clinically treatable through DBS, such as comorbidities of PD and other diseases with similar symptoms [45].
Patients being considered for device-assisted therapies must undergo evaluation by a specialized center’s multi-disciplinary team, which typically includes a functional neurosurgeon, an anesthesiologist, a movement disorder neurologist, and a neuropsychologist, as well as representatives from departments such as radiology, psychiatry, physical therapy, nursing, and social work.
Another factor to consider when selecting candidates for DBS is the patient’s responsiveness to levodopa, a common medication used to treat PD. Many studies have found that patients who are responsive to levodopa are more likely to also respond to DBS [46][47], while some others have found conflicting evidence [48][49]. The site of stimulation may affect the relationship between levodopa responsiveness and DBS efficacy, but the reason for this is not well understood. Lin et al. found a positive correlation between levodopa responsiveness and GPi-DBS efficacy (R2 = 0.283, p = 0.016), though STN DBS was more efficacious than GPi-DBS for levodopa-resistant tremor control [50]. There is no current indication of how medication for AD may interact with DBS treatment, but co-therapy to mitigate the side effects is certainly something future clinical trials could investigate. In the future, online tools may be developed to help improve the selection process for DBS candidates and provide more uniformity in the selection process. One study found that the use of an online tool called Stimulus to screen 3128 patients led to a significantly higher acceptance rate than conventional multi-disciplinary screening [51].

4. Procedure and Mechanism of Action

The DBS hardware includes multiconductor intracranial quadripolar electrodes, a programmable single- or dual-channel internal pulse generator with battery unit, and an extension cable connecting the DBS electrodes to the pulse generator [3].
The procedure involves stereotactic placement of electrodes in the target area, either unilaterally or bilaterally (Figure 2). This is the first stage of the procedure and is often performed while the patient is awake. In the second stage, the electrode and extension cable are tunneled under the skin to the infraclavicular area, where they are connected to the battery-powered pulse generator [28].
Figure 2. Electrode implantation for deep brain stimulation in Parkinson’s disease. Created using https://BioRender.com (Accessed on 19 December 2022).
When activated, the pulse generator delivers electric stimulation to the targeted area. The exact mechanism of action is not fully understood, but it is hypothesized that high-frequency DBS in PD suppresses GPi neuronal activity and efferent fiber pathways. This disrupts the flow of abnormal information through the cortico-basal ganglia circuits and downstream pathways, improving symptoms [52][53].
Overall, DBS as a procedure has come a long way since its initial development in the 1960s. Moreover, it is increasingly being trialed as an efficacious invasive procedure to alleviate the symptoms of many diseases. Additionally, more data are being generated on patient criteria which allows them to undergo ameliorative DBS treatment as well as the potential mechanisms by which DBS may affect different neurodegenerative diseases. Currently, the DBS only has regulatory approval in the treatment of PD.

References

  1. Parrent, A.G. History of Surgery for Movement Disorders. In Textbook of Stereotactic and Functional Neurosurgery; Springer: Berlin/Heidelberg, Germany, 2009; pp. 1467–1485.
  2. Burchiel, K.J. Thalamotomy for Movement Disorders. Neurosurg. Clin. N. Am. 1995, 6, 55–71.
  3. Miocinovic, S.; Somayajula, S.; Chitnis, S.; Vitek, J.L. History, Applications, and Mechanisms of Deep Brain Stimulation. JAMA Neurol. 2013, 70, 163–171.
  4. Spiegel, E.A. Stereoencephalotomy. J. Am. Med. Assoc. 1952, 148, 446–451.
  5. Ohye, C.; Kubota, K.; Hongo, T.; Nagao, T.; Narabayashi, H. Ventrolateral and Subventrolateral Thalamic Stimulation. Arch. Neurol. 1964, 11, 427–434.
  6. Premarket Approval (PMA), (n.d.). Available online: https://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfPMA/pma.cfm?id=P960009 (accessed on 23 December 2022).
  7. Mandybur, G. Deep Brain Stimulation (DBS) for Parkinson’s & Essential Tremor|Mayfield Brain & Spine, Cincinnati, (n.d.). Available online: https://mayfieldclinic.com/pe-dbs.htm (accessed on 13 December 2022).
  8. Deuschl, G.; Schade-Brittinger, C.; Krack, P.; Volkmann, J.; Schäfer, H.; Bötzel, K.; Daniels, C.; Deutschländer, A.; Dillmann, U.; Eisner, W.; et al. A Randomized Trial of Deep-Brain Stimulation for Parkinson’s Disease. N. Engl. J. Med. 2006, 355, 896–908.
  9. Xie, T.; Vigil, J.; MacCracken, E.; Gasparaitis, A.; Young, J.; Kang, W.; Bernard, J.; Warnke, P.; Kang, U.J. Low-frequency stimulation of STN-DBS reduces aspiration and freezing of gait in patients with PD. Neurology 2014, 84, 415–420.
  10. Blomstedt, P.; Persson, R.S.; Hariz, G.-M.; Linder, J.; Fredricks, A.; Häggström, B.; Philipsson, J.; Forsgren, L.; Hariz, M. Deep brain stimulation in the caudal zona incerta versus best medical treatment in patients with Parkinson’s disease: A randomised blinded evaluation. J. Neurol. Neurosurg. Psychiatry 2018, 89, 710–716.
  11. Baker, K.B.; Lee, J.Y.; Mavinkurve, G.; Russo, G.S.; Walter, B.; DeLong, M.R.; Bakay, R.A.; Vitek, J.L. Somatotopic organization in the internal segment of the globus pallidus in Parkinson’s disease. Exp. Neurol. 2010, 222, 219–225.
  12. Ossowska, K. Zona incerta as a therapeutic target in Parkinson’s disease. J. Neurol. 2019, 267, 591–606.
  13. Thevathasan, W.; Debu, B.; Aziz, T.; Bloem, B.R.; Blahak, C.; Butson, C.; Czernecki, V.; Foltynie, T.; Fraix, V.; Grabli, D.; et al. Pedunculopontine nucleus deep brain stimulation in Parkinson’s disease: A clinical review. Mov. Disord. 2017, 33, 10–20.
  14. Baizabal-Carvallo, J.F.; Kagnoff, M.N.; Jimenez-Shahed, J.; Fekete, R.; Jankovic, J. The safety and efficacy of thalamic deep brain stimulation in essential tremor: 10 years and beyond. J. Neurol. Neurosurg. Psychiatry 2013, 85, 567–572.
  15. Fytagoridis, A.; Sandvik, U.; Åström, M.; Bergenheim, T.; Blomstedt, P. Long term follow-up of deep brain stimulation of the caudal zona incerta for essential tremor. J. Neurol. Neurosurg. Psychiatry 2011, 83, 258–262.
  16. Vidailhet, M.; Jutras, M.-F.; Roze, E.; Grabli, D. Deep brain stimulation for dystonia. Handb. Clin. Neurol. 2013, 116, 167–187.
  17. Yu, X.-G.; Mao, Z.-Q.; Wang, X.; Xu, X.; Cui, Z.-Q.; Pan, L.-S.; Ning, X.-J.; Xu, B.-X.; Ma, L.; Ling, Z.-P.; et al. Partial improvement in performance of patients with severe Alzheimer’s disease at an early stage of fornix deep brain stimulation. Neural Regen. Res. 2018, 13, 2164–2172.
  18. Lozano, A.M.; Fosdick, L.; Chakravarty, M.M.; Leoutsakos, J.-M.; Munro, C.; Oh, E.; Drake, K.E.; Lyman, C.H.; Rosenberg, P.B.; Anderson, W.S.; et al. A Phase II Study of Fornix Deep Brain Stimulation in Mild Alzheimer’s Disease. J. Alzheimer’s Dis. 2016, 54, 777–787.
  19. Scharre, D.W.; Weichart, E.; Nielson, D.; Zhang, J.; Agrawal, P.; Sederberg, P.B.; Knopp, M.V.; Rezai, A.R.; Initiative, F.T.A.D.N. Deep Brain Stimulation of Frontal Lobe Networks to Treat Alzheimer’s Disease. J. Alzheimer’s Dis. 2018, 62, 621–633.
  20. Chakravarty, M.M.; Hamani, C.; Martinez-Canabal, A.; Ellegood, J.; Laliberté, C.; Nobrega, J.N.; Sankar, T.; Lozano, A.M.; Frankland, P.W.; Lerch, J.P. Deep brain stimulation of the ventromedial prefrontal cortex causes reorganization of neuronal processes and vasculature. Neuroimage 2016, 125, 422–427.
  21. Laxton, A.W.; Tang-Wai, D.F.; McAndrews, M.P.; Zumsteg, D.; Wennberg, R.; Keren, R.; Wherrett, J.; Naglie, G.; Hamani, C.; Smith, G.S.; et al. A phase I trial of deep brain stimulation of memory circuits in Alzheimer’s disease. Ann. Neurol. 2010, 68, 521–534.
  22. Kuhn, J.; Hardenacke, K.; Lenartz, D.; Gruendler, T.; Ullsperger, M.; Bartsch, C.; Mai, J.K.; Zilles, K.; Bauer, A.; Matusch, A.; et al. Deep brain stimulation of the nucleus basalis of Meynert in Alzheimer’s dementia. Mol. Psychiatry 2014, 20, 353–360.
  23. Velez-Lago, F.M.; Thompson, A.; Oyama, G.; Hardwick, A.; Sporrer, J.M.; Zeilman, P.; Foote, K.D.; Bowers, D.; Ward, H.E.; Sanchez-Ramos, J.; et al. Differential and Better Response to Deep Brain Stimulation of Chorea Compared to Dystonia in Huntington’s Disease. Ster. Funct. Neurosurg. 2013, 91, 129–133.
  24. Nair, G.; Evans, A.; Bear, R.E.; Velakoulis, D.; Bittar, R.G. The anteromedial GPi as a new target for deep brain stimulation in obsessive compulsive disorder. J. Clin. Neurosci. 2014, 21, 815–821.
  25. Huff, W.; Lenartz, D.; Schormann, M.; Lee, S.-H.; Kuhn, J.; Koulousakis, A.; Mai, J.; Daumann, J.; Maarouf, M.; Klosterkötter, J.; et al. Unilateral deep brain stimulation of the nucleus accumbens in patients with treatment-resistant obsessive-compulsive disorder: Outcomes after one year. Clin. Neurol. Neurosurg. 2010, 112, 137–143.
  26. Denys, D.; Mantione, M.; Figee, M.; Munckhof, P.V.D.; Koerselman, F.; Westenberg, H.; Bosch, A.; Schuurman, R. Deep Brain Stimulation of the Nucleus Accumbens for Treatment-Refractory Obsessive-Compulsive Disorder. Arch. Gen. Psychiatry 2010, 67, 1061–1068.
  27. Denys, D.; Graat, I.; Mocking, R.; de Koning, P.; Vulink, N.; Figee, M.; Ooms, P.; Mantione, M.; Munckhof, P.V.D.; Schuurman, R. Efficacy of Deep Brain Stimulation of the Ventral Anterior Limb of the Internal Capsule for Refractory Obsessive-Compulsive Disorder: A Clinical Cohort of 70 Patients. Am. J. Psychiatry 2020, 177, 265–271.
  28. Kammen, A.; Cavaleri, J.; Lam, J.; Frank, A.C.; Mason, X.; Choi, W.; Penn, M.; Brasfield, K.; Van Noppen, B.; Murray, S.B.; et al. Neuromodulation of OCD: A review of invasive and non-invasive methods. Front. Neurol. 2022, 13, 909264.
  29. Park, Y.-S.; Sammartino, F.; Young, N.A.; Corrigan, J.; Krishna, V.; Rezai, A.R. Anatomic Review of the Ventral Capsule/Ventral Striatum and the Nucleus Accumbens to Guide Target Selection for Deep Brain Stimulation for Obsessive-Compulsive Disorder. World Neurosurg. 2019, 126, 1–10.
  30. Greenberg, B.D.; A Gabriels, L.; A Malone, D.; Rezai, A.R.; Friehs, G.M.; Okun, M.; A Shapira, N.; Foote, K.; Cosyns, P.R.; Kubu, C.S.; et al. Deep brain stimulation of the ventral internal capsule/ventral striatum for obsessive-compulsive disorder: Worldwide experience. Mol. Psychiatry 2008, 15, 64–79.
  31. Li, N.; Baldermann, J.C.; Kibleur, A.; Treu, S.; Akram, H.; Elias, G.J.B.; Boutet, A.; Lozano, A.M.; Al-Fatly, B.; Strange, B.; et al. A unified connectomic target for deep brain stimulation in obsessive-compulsive disorder. Nat. Commun. 2020, 11, 3364.
  32. Chabardès, S.; Polosan, M.; Krack, P.; Bastin, J.; Krainik, A.; David, O.; Bougerol, T.; Benabid, A.L. Deep Brain Stimulation for Obsessive-Compulsive Disorder: Subthalamic Nucleus Target. World Neurosurg. 2012, 80, S31.e1–S31.e8.
  33. Germann, J.; Boutet, A.; Elias, G.J.; Gouveia, F.V.; Loh, A.; Giacobbe, P.; Bhat, V.; Kucharczyk, W.; Lozano, A.M. Brain Structures and Networks Underlying Treatment Response to Deep Brain Stimulation Targeting the Inferior Thalamic Peduncle in Obsessive-Compulsive Disorder. Ster. Funct. Neurosurg. 2022, 100, 236–243.
  34. Lee, D.J.; Dallapiazza, R.F.; De Vloo, P.; Elias, G.J.; Fomenko, A.; Boutet, A.; Giacobbe, P.; Lozano, A.M. Inferior thalamic peduncle deep brain stimulation for treatment-refractory obsessive-compulsive disorder: A phase 1 pilot trial. Brain Stimul. 2019, 12, 344–352.
  35. Luyten, L.; Hendrickx, S.; Raymaekers, S.; Gabriels, L.; Nuttin, B. Electrical stimulation in the bed nucleus of the stria terminalis alleviates severe obsessive-compulsive disorder. Mol. Psychiatry 2015, 21, 1272–1280.
  36. Mosley, P.E.; Windels, F.; Morris, J.; Coyne, T.; Marsh, R.; Giorni, A.; Mohan, A.; Sachdev, P.; O’leary, E.; Boschen, M.; et al. A randomised, double-blind, sham-controlled trial of deep brain stimulation of the bed nucleus of the stria terminalis for treatment-resistant obsessive-compulsive disorder. Transl. Psychiatry 2021, 11, 190.
  37. Raymaekers, S.; Vansteelandt, K.; Luyten, L.; Bervoets, C.; Demyttenaere, K.; Gabriels, L.; Nuttin, B. Long-term electrical stimulation of bed nucleus of stria terminalis for obsessive-compulsive disorder. Mol. Psychiatry 2016, 22, 931–934.
  38. Salanova, V. Deep brain stimulation for epilepsy. Epilepsy Behav. 2018, 88, 21–24.
  39. Malone, D.A., Jr.; Dougherty, D.D.; Rezai, A.R.; Carpenter, L.L.; Friehs, G.M.; Eskandar, E.N.; Rauch, S.L.; Rasmussen, S.A.; Machado, A.G.; Kubu, C.S.; et al. Deep Brain Stimulation of the Ventral Capsule/Ventral Striatum for Treatment-Resistant Depression. Biol. Psychiatry 2009, 65, 267–275.
  40. Bewernick, B.H.; Hurlemann, R.; Matusch, A.; Kayser, S.; Grubert, C.; Hadrysiewicz, B.; Axmacher, N.; Lemke, M.; Cooper-Mahkorn, D.; Cohen, M.X.; et al. Nucleus Accumbens Deep Brain Stimulation Decreases Ratings of Depression and Anxiety in Treatment-Resistant Depression. Biol. Psychiatry 2010, 67, 110–116.
  41. Baizabal-Carvallo, J.F.; Alonso-Juarez, M. Low-frequency deep brain stimulation for movement disorders. Park. Relat. Disord. 2016, 31, 14–22.
  42. di Biase, L.; Fasano, A. Low-frequency deep brain stimulation for Parkinson’s disease: Great expectation or false hope? Mov. Disord. 2016, 31, 962–967.
  43. Wyckhuys, T.; Raedt, R.; Vonck, K.; Wadman, W.; Boon, P. Comparison of hippocampal Deep Brain Stimulation with high (130Hz) and low frequency (5Hz) on afterdischarges in kindled rats. Epilepsy Res. 2010, 88, 239–246.
  44. Ramdhani, R.A.; Patel, A.; Swope, D.; Kopell, B.H. Early Use of 60 Hz Frequency Subthalamic Stimulation in Parkinson’s Disease: A Case Series and Review. Neuromodulation Technol. Neural Interface 2015, 18, 664–669.
  45. Okun, M.S.; Foote, K.D. Parkinson’s disease DBS: What, when, who and why? The time has come to tailor DBS targets. Expert Rev. Neurother. 2010, 10, 1847–1857.
  46. Rodriguez, R.L.; Fernandez, H.H.; Haq, I.; Okun, M. Pearls in Patient Selection for Deep Brain Stimulation. Neurologist 2007, 13, 253–260.
  47. Ghika, J.; Villemure, J.-G.; Fankhauser, H.; Favre, J.; Assal, G.; Ghika-Schmid, F. Efficiency and safety of bilateral contemporaneous pallidal stimulation (deep brain stimulation) in levodopa-responsive patients with Parkinson’s disease with severe motor fluctuations: A 2-year follow-up review. J. Neurosurg. 1998, 89, 713–718.
  48. Yamada, K.; Hamasaki, T.; Kuratsu, J.-I. Thalamic stimulation alleviates levodopa-resistant rigidity in a patient with non-Parkinson’s disease parkinsonian syndrome. J. Clin. Neurosci. 2014, 21, 882–884.
  49. Chang, S.J.; Cajigas, I.; Guest, J.D.; Noga, B.R.; Widerström-Noga, E.; Haq, I.; Fisher, L.; Luca, C.C.; Jagid, J.R. MR Tractography-Based Targeting and Physiological Identification of the Cuneiform Nucleus for Directional DBS in a Parkinson’s Disease Patient With Levodopa-Resistant Freezing of Gait. Front. Hum. Neurosci. 2021, 15, 676755.
  50. Lin, Z.; Zhang, X.; Wang, L.; Zhang, Y.; Zhou, H.; Sun, Q.; Sun, B.; Huang, P.; Li, D. Revisiting the L-Dopa Response as a Predictor of Motor Outcomes After Deep Brain Stimulation in Parkinson’s Disease. Front. Hum. Neurosci. 2021, 15, 604433.
  51. Wächter, T.; Mínguez-Castellanos, A.; Valldeoriola, F.; Herzog, J.; Stoevelaar, H. A tool to improve pre-selection for deep brain stimulation in patients with Parkinson’s disease. J. Neurol. 2010, 258, 641–646.
  52. Emamikhah, M.; Akhoundi, F.H.; Rohani, M. Mechanism of Deep Brain Stimulation. Handb. Neuromodulation 2022, 1, 245–264.
  53. Okun, M.S. Deep-Brain Stimulation for Parkinson’s Disease. N. Engl. J. Med. 2012, 367, 1529–1538.
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