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Treatment of Persistent Hemiballism with Deep Brain Stimulation of the Globus Pallidus Internus: Case Report and Literature Review
Journal Pre-proof Case report and literature review of treatment of persistent hemiballism with deep brain stimulation of the globus pallidus internus (GPi-DBS) Somnath V. Ganapa, B.S., Margish D. Ramani, B.S., Oladotun O. Ebunlomo, B.A., Raphia K. Rahman, B.A., M.B.S, Yehuda Herschman, M.D., Antonios Mammis, M.D. PII:
S1878-8750(19)32415-5
DOI:
https://doi.org/10.1016/j.wneu.2019.08.247
Reference:
WNEU 13284
To appear in:
World Neurosurgery
Received Date: 9 August 2019 Accepted Date: 30 August 2019
Please cite this article as: Ganapa SV, Ramani MD, Ebunlomo OO, Rahman RK, Herschman Y, Mammis A, Case report and literature review of treatment of persistent hemiballism with deep brain stimulation of the globus pallidus internus (GPi-DBS), World Neurosurgery (2019), doi: https:// doi.org/10.1016/j.wneu.2019.08.247. This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. © 2019 Elsevier Inc. All rights reserved.
Title: Case report and literature review of treatment of persistent hemiballism with deep brain stimulation of the globus pallidus internus (GPi-DBS) Authors: Somnath V. Ganapa, B.S.a,b; Margish D. Ramani a,c, B.S.; Oladotun O Ebunlomo, B.A. a,d; Raphia K Rahman, B.A., M.B.S. a,e; Yehuda Herschman, M.D. a,f; Antonios Mammis, M.D. a,g a
Department of Neurological Surgery, Rutgers New Jersey Medical School, 90 Bergen Street Newark, NJ 07101-1709. b [email protected] c [email protected] d [email protected] e [email protected] f [email protected] g [email protected] Corresponding author: Somnath V. Ganapa, [email protected] Keywords: persistent hemiballism, deep brain stimulation, globus pallidus internus, DBS, GPi, DBS-GPi, case report Short title: Title as listed is fine as is.
Introduction Hemiballism is a rare hyperkinetic movement disorder characterized by involuntary, high amplitude, unilateral flailing of either upper or lower extremities, or both. Hemiballism typically results from lesions or physiological malfunctioning of the thalamus, subthalamic nucleus (STN), globus pallidus internus (GPi), or other affiliated deep brain regions.1,2 Damage to these brain regions can be caused by infections, neurovascular events, trauma, or severe cases of nonketotic hyperglycemia.1 There are also a few cases of hemiballism secondary to implantation of surgical electrodes to treat other neurological illnesses such as Parkinson’s Disease.3 Although most patients with hemiballism improve without intervention, current treatment options for persistent hemiballism include dopamine blockers, anticonvulsants, intrathecal baclofen (ITB) therapy, botulinum injections, tetrabenazine, antipsychotics, and deep brain stimulation (DBS).4-8 In the case of hemiballism refractory to pharmaceutical interventions, DBS is an effective primary neurosurgical treatment.3 DBS involves the implantation of electrodes to stimulate neurons of a specific brain target. DBS targets for hemiballism include the thalamus, the subthalamic nucleus (STN), and the globus pallidus internus (GPi). By targeting these brain regions, DBS is thought to modulate voluntary movement by altering the pathophysiologic state of the basal ganglia. Primates and humans suffering from hemiballism demonstrate reduced glutaminergic drive from the STN, which decreases the neuronal firing of the GPi neurons. In turn, decreased firing of GPi neurons decreases the inhibitory signaling to the thalamus and brainstem. The basis of hemiballism and similar dystonias was believed to be the inability of the GPi neurons to inhibit the thalamus, resulting in involuntary movements.9 However, ablation of the GPi via pallidotomy has been found to resolve hemiballistic symptoms. Pallidotomy would abolish the firing of GPi neurons completely, suggesting that it is not a decreased rate of firing that causes hemiballism, but possibly an irregular firing of these neurons.10 In this paper, we describe a patient who sustained a posterior cerebral artery (PCA) ischemic stroke that eventually led to uncontrolled hemiballism, which was then successfully treated by unilateral GPi stimulation. We include video recordings depicting patient pre-op, intra-op with stimulation off, and intra-op with stimulation on. We also review published cases of hemiballism treated by GPi-DBS, which support the claim that DBS is an effective method for treating hemiballism. Case Report A 46-year-old man with a past medical history of hypertension and diabetes suffered an ischemic stroke involving the right posterior cerebral artery (PCA). Following the stroke, the patient had a left-sided hemiplegia, which progressed to high-amplitude,
low-frequency movement of the left arm consistent with hemiballism. This movement can be seen on video recording. Five years post-stroke, hemiballistic and hyperkinetic movements had been refractory to treatment with prescribed risperidone. The decision was made to place a deep brain stimulator in the right GPi to control the hemiballistic movements. A pulse generator was installed after one week. Patient was seen on follow-up one week after his pulse generator was placed for device programming. Postoperative course resulted in substantial alleviation of hemiballistic movements and increased motor control necessary to complete motor tasks. He was found to tolerate stimulation and did not have any side effects. More recent follow-up is missing because patient returned to native country and contact was lost. Discussion A thorough analysis of published case studies provides ample evidence that globus pallidus internus deep brain stimulation (GPi-DBS) is an effective method for treating hemiballism. The case studies examined support that GPi-DBS can achieve long-term alleviation of symptoms with minimal adverse effects. Including our case report, we found a total of 6 patients with hemiballism who were treated with GPi-DBS in the literature. The cause of hemiballism in each of these cases are among the most common etiologies, such as ischemic or hemorrhagic stroke and nonketotic hyperglycemia.11 In Hasegawa et al., a 56-year-old male suffered from hemorrhage in the right subthalamic nucleus, resulting in left-sided hemiballism. After 3 years of unsuccessful medical therapy at maximally tolerated doses, patient was referred to functional neurosurgery. On physical examination, when the patient attempted to use his left arm, it repeatedly and involuntarily assumed a position resembling waiter’s tip. Additionally, patient exhibited milder dystonic and choreic movements of the left leg. A DBS electrode was placed in the right GPi leading to immediate improvement of symptoms. At 15 months follow up, the patient’s symptoms had improved from disabling left arm movement to purposeful usage (e.g. holding a pan, opening doors, walking) with residual left wrist dystonia.12 In Oyama et al., a 38-year-old male with previous history of Parkinson’s disease was treated with bilateral STN-DBS. Ten months after successful control of symptoms, the patient experienced sudden-onset, severe left arm and leg hemiballism. MRI revealed a right-sided lesion adjacent to the placement of the right-sided electrode. In order to control left-sided hemiballism, a right-sided GPi-DBS electrode was implanted and successfully controlled symptoms upon follow-up within a week of implantation. This case report suggests GPi-DBS may be a viable therapeutic option for the treatment of hemiballism refractory to bilateral STN-DBS treatment of Parkinson’s disease.2
Similarly, in Pabaney et al., a 54-year-old male with previous history of Parkinson’s disease was also successfully treated with bilateral STN-DBS. 3 months after STN-DBS electrodes were implanted, patient fell and suffered traumatic brain injury, resulting in right-sided hemiballism involving the arms and legs within minutes. After 2 weeks of failed control of hemiballism with haloperidol, patient was referred to neurosurgery. The left STN-DBS electrode was replaced with a left GPI-DBS electrode. Additionally, the right STN-DBS electrode was found to be dislocated on MRI and was therefore moved to its original position during the same surgery. While the patient’s hemiballism significantly improved, over the next few weeks, the patient developed symptoms of multiple system atrophy (MSA), which was confirmed with MRI.13 In Son et al., a 46-year-old female with an 11 year history of type II diabetes mellitus presented with progressively worsening left-sided hemiballism over two weeks, triggered by an episode of heavy lifting. On evaluation, the patient was found to have a blood glucose level of 536 mg/dL and a serum osmolarity of 335 mOsm/kg, and was diagnosed with nonketotic hyperglycemic hyperosmolar syndrome. After three months of insulin treatment, hemiballism improved but remained disabling. Patient received GPi-DBS treatment, resulting in gross elimination of hemiballism upon evaluation 16 months after surgery.14 Ramirez-Zamora et al. describes a 53-year-old female presenting with progressively worsening hemiballism in her left arm secondary to peripartum right thalamic cerebral infarction in her 30s. Her symptoms were refractory to multiple medications so the decision was made to implant unilateral right GPi electrode for DBS. At follow-up 28 months after implantation, hemiballism was nearly completely eliminated.15 Throughout the literature, there is a collective agreement from the authors that GPi can be an optimal target to address hemiballism after neuroleptics have failed to resolve the motor disorder. Improved control of ballistic movements should be visible immediately after the procedure has concluded. Additionally, time between onset of hemiballism and implantation of GPi-DBS electrode did not seem to influence the efficacy of treatment. Further research into GPi-DBS can lead to better treatment of dyskinesias, greater flexibility for medication adjustments, and better control of symptoms. Furthermore, it is still unclear which of the three main targets for hemiballism (thalamus, STN, GPi) is the most effective for controlling hemiballism. While stimulation of any of the three targets may alleviate symptoms, one variable to consider is the varying voltage necessary to stimulate the brain region of interest in order to control hemiballism. In one case report of a 52-year-old woman with hemiballism, thalamic stimulation required clearly less voltage than pallidal stimulation in order to completely control symptoms16 However, whether the lower threshold for symptom control via thalamic stimulation is specific to this case or generally true remains unclear.
Conclusion Evidence gathered from the literature indicate that GPI-DBS is an effective treatment for hemiballism, especially after neuroleptics have failed. Results from various case studies of GPI-DBS treated hemiballism reveal improved motor ability and decreased dyskinesia, though the degree of improvement may vary. Patients experienced an improved gait, motor function and quality of life. More studies are required to establish which DBS target requires the least amount of stimulation to treat hemiballism.
References 1. 2.
3. 4. 5. 6. 7.
8. 9. 10. 11. 12.
13.
Shannon KM. Hemiballismus. Curr Treat Options Neurol. 2005;7(3):203-210. Oyama G, Maling N, Avila-Thompson A, et al. Rescue GPi-DBS for a Strokeassociated Hemiballism in a Patient with STN-DBS. Tremor Other Hyperkinet Mov (N Y). 2014;4. Franzini A, Cordella R, Rizzi M, et al. Deep brain stimulation in critical care conditions. J Neural Transm (Vienna). 2014;121(4):391-398. Driver-Dunckley E, Evidente VG. Hemichorea-hemiballismus may respond to topiramate. Clin Neuropharmacol. 2005;28(3):142-144. Postuma RB, Lang AE. Hemiballism: revisiting a classic disorder. Lancet Neurol. 2003;2(11):661-668. Francisco GE. Successful treatment of posttraumatic hemiballismus with intrathecal baclofen therapy. Am J Phys Med Rehabil. 2006;85(9):779-782. Mukand JA, Fitzsimmons C, Wennemer HK, Carrillo A, Cai C, Bailey KM. Olanzapine for the treatment of hemiballismus: A case report. Arch Phys Med Rehabil. 2005;86(3):587-590. Sitburana O, Ondo WG. Tetrabenazine for hyperglycemic-induced hemichoreahemiballismus. Mov Disord. 2006;21(11):2023-2025. Chiken S, Nambu A. Mechanism of Deep Brain Stimulation: Inhibition, Excitation, or Disruption? Neuroscientist. 2016;22(3):313-322. Goto T, Hashimoto T, Hirayama S, Kitazawa K. Pallidal neuronal activity in diabetic hemichorea-hemiballism. Mov Disord. 2010;25(9):1295-1297. Hawley JS, Weiner WJ. Hemiballismus: current concepts and review. Parkinsonism Relat Disord. 2012;18(2):125-129. Hasegawa H, Mundil N, Samuel M, Jarosz J, Ashkan K. The treatment of persistent vascular hemidystonia-hemiballismus with unilateral GPi deep brain stimulation. Mov Disord. 2009;24(11):1697-1698. Pabaney A, Ali R, Lewitt PA, Sidiropoulos C, Schwalb JM. Successful Management of Hemorrhage-Associated Hemiballism After Subthalamic Nucleus
14.
15.
16.
Deep Brain Stimulation with Pallidal Stimulation: a Case Report. World Neurosurg. 2015;84(4):1176.e1171-1173. Son BC, Choi JG, Ko HC. Globus Pallidus Internus Deep Brain Stimulation for Disabling Diabetic Hemiballism/Hemichorea. Case Rep Neurol Med. 2017;2017:2165905. Ramirez-Zamora A, Eisinger RS, Haider SA, et al. Pallidal deep brain stimulation and intraoperative neurophysiology for treatment of poststroke hemiballism. Ann Clin Transl Neurol. 2018;5(7):865-869. Capelle HH, Kinfe TM, Krauss JK. Deep brain stimulation for treatment of hemichorea-hemiballism after craniopharyngioma resection: long-term follow-up. J Neurosurg. 2011;115(5):966-970.
Figure 1. Preoperative axial (A) and coronal (B) T2-weighted MR images demonstrating right-sided infarct of the thalamus and subthalamic nucleus. Postoperative axial (C) and coronal (D) CT images depicting DBS lead in the GPi.
DBS – Deep brain stimulation GPi – Globus pallidus internus GPI-DBS – Globus pallidus internus deep brain stimulation ITB – Intrathecal baclofen MSA – Multiple system atrophy PCA – Posterior cerebral artery STN – Subthalamic nucleus STN-DBS – Subthalamic nucleus deep brain stimulation
S1878-8750(19)32415-5
DOI:
https://doi.org/10.1016/j.wneu.2019.08.247
Reference:
WNEU 13284
To appear in:
World Neurosurgery
Received Date: 9 August 2019 Accepted Date: 30 August 2019
Please cite this article as: Ganapa SV, Ramani MD, Ebunlomo OO, Rahman RK, Herschman Y, Mammis A, Case report and literature review of treatment of persistent hemiballism with deep brain stimulation of the globus pallidus internus (GPi-DBS), World Neurosurgery (2019), doi: https:// doi.org/10.1016/j.wneu.2019.08.247. This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. © 2019 Elsevier Inc. All rights reserved.
Title: Case report and literature review of treatment of persistent hemiballism with deep brain stimulation of the globus pallidus internus (GPi-DBS) Authors: Somnath V. Ganapa, B.S.a,b; Margish D. Ramani a,c, B.S.; Oladotun O Ebunlomo, B.A. a,d; Raphia K Rahman, B.A., M.B.S. a,e; Yehuda Herschman, M.D. a,f; Antonios Mammis, M.D. a,g a
Department of Neurological Surgery, Rutgers New Jersey Medical School, 90 Bergen Street Newark, NJ 07101-1709. b [email protected] c [email protected] d [email protected] e [email protected] f [email protected] g [email protected] Corresponding author: Somnath V. Ganapa, [email protected] Keywords: persistent hemiballism, deep brain stimulation, globus pallidus internus, DBS, GPi, DBS-GPi, case report Short title: Title as listed is fine as is.
Introduction Hemiballism is a rare hyperkinetic movement disorder characterized by involuntary, high amplitude, unilateral flailing of either upper or lower extremities, or both. Hemiballism typically results from lesions or physiological malfunctioning of the thalamus, subthalamic nucleus (STN), globus pallidus internus (GPi), or other affiliated deep brain regions.1,2 Damage to these brain regions can be caused by infections, neurovascular events, trauma, or severe cases of nonketotic hyperglycemia.1 There are also a few cases of hemiballism secondary to implantation of surgical electrodes to treat other neurological illnesses such as Parkinson’s Disease.3 Although most patients with hemiballism improve without intervention, current treatment options for persistent hemiballism include dopamine blockers, anticonvulsants, intrathecal baclofen (ITB) therapy, botulinum injections, tetrabenazine, antipsychotics, and deep brain stimulation (DBS).4-8 In the case of hemiballism refractory to pharmaceutical interventions, DBS is an effective primary neurosurgical treatment.3 DBS involves the implantation of electrodes to stimulate neurons of a specific brain target. DBS targets for hemiballism include the thalamus, the subthalamic nucleus (STN), and the globus pallidus internus (GPi). By targeting these brain regions, DBS is thought to modulate voluntary movement by altering the pathophysiologic state of the basal ganglia. Primates and humans suffering from hemiballism demonstrate reduced glutaminergic drive from the STN, which decreases the neuronal firing of the GPi neurons. In turn, decreased firing of GPi neurons decreases the inhibitory signaling to the thalamus and brainstem. The basis of hemiballism and similar dystonias was believed to be the inability of the GPi neurons to inhibit the thalamus, resulting in involuntary movements.9 However, ablation of the GPi via pallidotomy has been found to resolve hemiballistic symptoms. Pallidotomy would abolish the firing of GPi neurons completely, suggesting that it is not a decreased rate of firing that causes hemiballism, but possibly an irregular firing of these neurons.10 In this paper, we describe a patient who sustained a posterior cerebral artery (PCA) ischemic stroke that eventually led to uncontrolled hemiballism, which was then successfully treated by unilateral GPi stimulation. We include video recordings depicting patient pre-op, intra-op with stimulation off, and intra-op with stimulation on. We also review published cases of hemiballism treated by GPi-DBS, which support the claim that DBS is an effective method for treating hemiballism. Case Report A 46-year-old man with a past medical history of hypertension and diabetes suffered an ischemic stroke involving the right posterior cerebral artery (PCA). Following the stroke, the patient had a left-sided hemiplegia, which progressed to high-amplitude,
low-frequency movement of the left arm consistent with hemiballism. This movement can be seen on video recording. Five years post-stroke, hemiballistic and hyperkinetic movements had been refractory to treatment with prescribed risperidone. The decision was made to place a deep brain stimulator in the right GPi to control the hemiballistic movements. A pulse generator was installed after one week. Patient was seen on follow-up one week after his pulse generator was placed for device programming. Postoperative course resulted in substantial alleviation of hemiballistic movements and increased motor control necessary to complete motor tasks. He was found to tolerate stimulation and did not have any side effects. More recent follow-up is missing because patient returned to native country and contact was lost. Discussion A thorough analysis of published case studies provides ample evidence that globus pallidus internus deep brain stimulation (GPi-DBS) is an effective method for treating hemiballism. The case studies examined support that GPi-DBS can achieve long-term alleviation of symptoms with minimal adverse effects. Including our case report, we found a total of 6 patients with hemiballism who were treated with GPi-DBS in the literature. The cause of hemiballism in each of these cases are among the most common etiologies, such as ischemic or hemorrhagic stroke and nonketotic hyperglycemia.11 In Hasegawa et al., a 56-year-old male suffered from hemorrhage in the right subthalamic nucleus, resulting in left-sided hemiballism. After 3 years of unsuccessful medical therapy at maximally tolerated doses, patient was referred to functional neurosurgery. On physical examination, when the patient attempted to use his left arm, it repeatedly and involuntarily assumed a position resembling waiter’s tip. Additionally, patient exhibited milder dystonic and choreic movements of the left leg. A DBS electrode was placed in the right GPi leading to immediate improvement of symptoms. At 15 months follow up, the patient’s symptoms had improved from disabling left arm movement to purposeful usage (e.g. holding a pan, opening doors, walking) with residual left wrist dystonia.12 In Oyama et al., a 38-year-old male with previous history of Parkinson’s disease was treated with bilateral STN-DBS. Ten months after successful control of symptoms, the patient experienced sudden-onset, severe left arm and leg hemiballism. MRI revealed a right-sided lesion adjacent to the placement of the right-sided electrode. In order to control left-sided hemiballism, a right-sided GPi-DBS electrode was implanted and successfully controlled symptoms upon follow-up within a week of implantation. This case report suggests GPi-DBS may be a viable therapeutic option for the treatment of hemiballism refractory to bilateral STN-DBS treatment of Parkinson’s disease.2
Similarly, in Pabaney et al., a 54-year-old male with previous history of Parkinson’s disease was also successfully treated with bilateral STN-DBS. 3 months after STN-DBS electrodes were implanted, patient fell and suffered traumatic brain injury, resulting in right-sided hemiballism involving the arms and legs within minutes. After 2 weeks of failed control of hemiballism with haloperidol, patient was referred to neurosurgery. The left STN-DBS electrode was replaced with a left GPI-DBS electrode. Additionally, the right STN-DBS electrode was found to be dislocated on MRI and was therefore moved to its original position during the same surgery. While the patient’s hemiballism significantly improved, over the next few weeks, the patient developed symptoms of multiple system atrophy (MSA), which was confirmed with MRI.13 In Son et al., a 46-year-old female with an 11 year history of type II diabetes mellitus presented with progressively worsening left-sided hemiballism over two weeks, triggered by an episode of heavy lifting. On evaluation, the patient was found to have a blood glucose level of 536 mg/dL and a serum osmolarity of 335 mOsm/kg, and was diagnosed with nonketotic hyperglycemic hyperosmolar syndrome. After three months of insulin treatment, hemiballism improved but remained disabling. Patient received GPi-DBS treatment, resulting in gross elimination of hemiballism upon evaluation 16 months after surgery.14 Ramirez-Zamora et al. describes a 53-year-old female presenting with progressively worsening hemiballism in her left arm secondary to peripartum right thalamic cerebral infarction in her 30s. Her symptoms were refractory to multiple medications so the decision was made to implant unilateral right GPi electrode for DBS. At follow-up 28 months after implantation, hemiballism was nearly completely eliminated.15 Throughout the literature, there is a collective agreement from the authors that GPi can be an optimal target to address hemiballism after neuroleptics have failed to resolve the motor disorder. Improved control of ballistic movements should be visible immediately after the procedure has concluded. Additionally, time between onset of hemiballism and implantation of GPi-DBS electrode did not seem to influence the efficacy of treatment. Further research into GPi-DBS can lead to better treatment of dyskinesias, greater flexibility for medication adjustments, and better control of symptoms. Furthermore, it is still unclear which of the three main targets for hemiballism (thalamus, STN, GPi) is the most effective for controlling hemiballism. While stimulation of any of the three targets may alleviate symptoms, one variable to consider is the varying voltage necessary to stimulate the brain region of interest in order to control hemiballism. In one case report of a 52-year-old woman with hemiballism, thalamic stimulation required clearly less voltage than pallidal stimulation in order to completely control symptoms16 However, whether the lower threshold for symptom control via thalamic stimulation is specific to this case or generally true remains unclear.
Conclusion Evidence gathered from the literature indicate that GPI-DBS is an effective treatment for hemiballism, especially after neuroleptics have failed. Results from various case studies of GPI-DBS treated hemiballism reveal improved motor ability and decreased dyskinesia, though the degree of improvement may vary. Patients experienced an improved gait, motor function and quality of life. More studies are required to establish which DBS target requires the least amount of stimulation to treat hemiballism.
References 1. 2.
3. 4. 5. 6. 7.
8. 9. 10. 11. 12.
13.
Shannon KM. Hemiballismus. Curr Treat Options Neurol. 2005;7(3):203-210. Oyama G, Maling N, Avila-Thompson A, et al. Rescue GPi-DBS for a Strokeassociated Hemiballism in a Patient with STN-DBS. Tremor Other Hyperkinet Mov (N Y). 2014;4. Franzini A, Cordella R, Rizzi M, et al. Deep brain stimulation in critical care conditions. J Neural Transm (Vienna). 2014;121(4):391-398. Driver-Dunckley E, Evidente VG. Hemichorea-hemiballismus may respond to topiramate. Clin Neuropharmacol. 2005;28(3):142-144. Postuma RB, Lang AE. Hemiballism: revisiting a classic disorder. Lancet Neurol. 2003;2(11):661-668. Francisco GE. Successful treatment of posttraumatic hemiballismus with intrathecal baclofen therapy. Am J Phys Med Rehabil. 2006;85(9):779-782. Mukand JA, Fitzsimmons C, Wennemer HK, Carrillo A, Cai C, Bailey KM. Olanzapine for the treatment of hemiballismus: A case report. Arch Phys Med Rehabil. 2005;86(3):587-590. Sitburana O, Ondo WG. Tetrabenazine for hyperglycemic-induced hemichoreahemiballismus. Mov Disord. 2006;21(11):2023-2025. Chiken S, Nambu A. Mechanism of Deep Brain Stimulation: Inhibition, Excitation, or Disruption? Neuroscientist. 2016;22(3):313-322. Goto T, Hashimoto T, Hirayama S, Kitazawa K. Pallidal neuronal activity in diabetic hemichorea-hemiballism. Mov Disord. 2010;25(9):1295-1297. Hawley JS, Weiner WJ. Hemiballismus: current concepts and review. Parkinsonism Relat Disord. 2012;18(2):125-129. Hasegawa H, Mundil N, Samuel M, Jarosz J, Ashkan K. The treatment of persistent vascular hemidystonia-hemiballismus with unilateral GPi deep brain stimulation. Mov Disord. 2009;24(11):1697-1698. Pabaney A, Ali R, Lewitt PA, Sidiropoulos C, Schwalb JM. Successful Management of Hemorrhage-Associated Hemiballism After Subthalamic Nucleus
14.
15.
16.
Deep Brain Stimulation with Pallidal Stimulation: a Case Report. World Neurosurg. 2015;84(4):1176.e1171-1173. Son BC, Choi JG, Ko HC. Globus Pallidus Internus Deep Brain Stimulation for Disabling Diabetic Hemiballism/Hemichorea. Case Rep Neurol Med. 2017;2017:2165905. Ramirez-Zamora A, Eisinger RS, Haider SA, et al. Pallidal deep brain stimulation and intraoperative neurophysiology for treatment of poststroke hemiballism. Ann Clin Transl Neurol. 2018;5(7):865-869. Capelle HH, Kinfe TM, Krauss JK. Deep brain stimulation for treatment of hemichorea-hemiballism after craniopharyngioma resection: long-term follow-up. J Neurosurg. 2011;115(5):966-970.
Figure 1. Preoperative axial (A) and coronal (B) T2-weighted MR images demonstrating right-sided infarct of the thalamus and subthalamic nucleus. Postoperative axial (C) and coronal (D) CT images depicting DBS lead in the GPi.
DBS – Deep brain stimulation GPi – Globus pallidus internus GPI-DBS – Globus pallidus internus deep brain stimulation ITB – Intrathecal baclofen MSA – Multiple system atrophy PCA – Posterior cerebral artery STN – Subthalamic nucleus STN-DBS – Subthalamic nucleus deep brain stimulation