Original Article
Deep-Brain Stimulation of the Subthalamic Nucleus or the Pars Interna of the Globus Pallidus in Parkinson's Disease
N Engl J Med 2001; 345:956-963September 27, 2001
- Abstract
Background
Increased neuronal activity in the subthalamic nucleus and the pars interna of the globus pallidus is thought to account for motor dysfunction in patients with Parkinson's disease. Although creating lesions in these structures improves motor function in monkeys with induced parkinsonism and patients with Parkinson's disease, such lesions are associated with neurologic deficits, particularly when they are created bilaterally. Deep-brain stimulation simulates the effects of a lesion without destroying brain tissue.
Methods
We performed a prospective, double-blind, crossover study in patients with advanced Parkinson's disease, in whom electrodes were implanted in the subthalamic nucleus or pars interna of the globus pallidus and who then underwent bilateral high-frequency deep-brain stimulation. We compared scores on the motor portion of the Unified Parkinson's Disease Rating Scale when the stimulation was randomly assigned to be turned on or off. We performed unblinded evaluations of motor function preoperatively and one, three, and six months postoperatively.
Results
Electrodes were implanted bilaterally in 96 patients in the subthalamic-nucleus group and 38 patients in the globus-pallidus group. Three months after the procedures were performed, double-blind, crossover evaluations demonstrated that stimulation of the subthalamic nucleus was associated with a median improvement in the motor score (as compared with no stimulation) of 49 percent, and stimulation of the pars interna of the globus pallidus with a median improvement of 37 percent (P<0.001 for both comparisons). Between the preoperative and six-month visits, the percentage of time during the day that patients had good mobility without involuntary movements increased from 27 percent to 74 percent (P<0.001) with subthalamic stimulation and from 28 percent to 64 percent (P<0.001) with pallidal stimulation. Adverse events included intracranial hemorrhage in seven patients and infection necessitating removal of the leads in two.
Conclusions
Bilateral stimulation of the subthalamic nucleus or pars interna of the globus pallidus is associated with significant improvement in motor function in patients with Parkinson's disease whose condition cannot be further improved with medical therapy.
Media in This Article
Figure 1
The Mean Percentage of Time during Waking Hours with Poor Mobility (the “Off” State), Good Mobility with Dyskinesia (the “On” State with Dyskinesia), and Good Mobility without Dyskinesia (the “On” State without Dyskinesia) at Base Line and Six Months after the Implantation of Electrodes for Bilateral Stimulation of Either the Subthalamic Nucleus or the Pars Interna of the Globus Pallidus.Table 1
Base-Line Characteristics of the 134 Patients with Bilateral Implants and Stimulation Settings at the Last Follow-up Visit.Article Activity
- Article
Levodopa is the mainstay of treatment for Parkinson's disease.1 However, long-term levodopa treatment is complicated by involuntary movements known as dyskinesia and motor fluctuations in which patients cycle between periods of good mobility (“on” periods) and impaired mobility (“off” periods).2 These complications result in disability that cannot be satisfactorily controlled by medical therapy in the majority of patients. Advances in understanding of the pathophysiology of the basal ganglia have provided opportunities for new therapeutic strategies to manage these problems.3-5 In animal models of Parkinson's disease, neuronal activity is increased in the subthalamic nucleus and pars interna of the globus pallidus,6 and lesions of these structures result in marked improvement in motor function.6-8 These findings have led to the development of surgical procedures for Parkinson's disease that target the subthalamic nucleus and pars interna of the globus pallidus.9,10
In patients with Parkinson's disease, the creation of lesions in the pars interna of the globus pallidus (pallidotomy) improves contralateral dyskinesia and provides moderate antiparkinsonian benefits.11,12 However, pallidotomy necessitates making a destructive brain lesion and entails the risk of inducing neurologic deficits, particularly with bilateral procedures.13 The creation of lesions in the subthalamic nucleus also provides benefits to patients,14 but is associated with the risk of hemiballismus.15 Accordingly, physicians have been reluctant to perform bilateral pallidotomy or subthalamotomy.10 High-frequency deep-brain stimulation of specific brain targets simulates the effect of a lesion without deliberately damaging the brain.16 Deep-brain stimulation of the thalamus has been shown to control tremor17 but not other, more disabling, features of Parkinson's disease. Studies in small numbers of patients with Parkinson's disease suggest that stimulation of the subthalamic nucleus and pars interna of the globus pallidus can improve the full constellation of parkinsonian motor features.18-22 We evaluated the results of bilateral pallidal or subthalamic stimulation in patients with advanced Parkinson's disease.
Methods
We performed a six-month, prospective, multicenter trial of bilateral deep-brain stimulation of the subthalamic nucleus or pars interna of the globus pallidus in patients with advanced Parkinson's disease. The study included a double-blind, randomized, crossover evaluation of the immediate effects of stimulation three months after implantation of the electrodes; unblinded evaluations of motor function two weeks before and one, three, and six months after implantation; and assessments of motor status with the use of a home diary.
Patients
The ages of the patients ranged from 30 to 75 years. The criteria for inclusion were the presence of at least two cardinal features of parkinsonism (tremor, rigidity, and bradykinesia), a good response to levodopa, a minimal score of 30 points on the motor portion of the Unified Parkinson's Disease Rating Scale (UPDRS) when the patient has been without medication for approximately 12 hours (scores on this scale range from 0 to 108; higher values indicate greater severity of symptoms23), and motor complications that could not be controlled with pharmacologic therapy. The criteria for exclusion were major psychiatric illness, cognitive impairment, other substantial medical problems or laboratory abnormalities, presence of a cardiac pacemaker, and previous intracranial surgery. The protocol was approved by the institutional review board of each participating center. All patients gave written informed consent.
Surgical Technique
The choice of the target site was determined at each center according to the experience and preference of the investigator. The target was identified by a combination of neuroimaging, microelectrode recording, and stimulation techniques.16-22 A permanent electrode (Medtronic model 3387 or 3389, Medtronic, Minneapolis) containing four contact sites was implanted with the patient under local anesthesia and was connected to a pulse generator (Medtronic model 7424) that was placed subcutaneously in the subclavicular area with the patient under general anesthesia. The procedure was repeated on the opposite side of the brain either at the same time or within three months. Postoperatively, adjustment of medication was permitted if parkinsonism worsened or adverse events occurred. Levodopa dose equivalents were calculated as follows: 100 mg of standard levodopa equals 133 mg of controlled-release levodopa equals 10 mg of bromocriptine equals 1 mg of pergolide.
Stimulation Settings
The pulse generator could be programmed with respect to electrode contact (four sites), polarity (monopolar or bipolar), frequency (up to 185 Hz), voltage (up to 10.5 V), and pulse width (up to 450 μsec). The stimulation settings were selected to maximize clinical benefit and minimize side effects. Adjustments could be performed at any time throughout the study.
Evaluations
Methods of evaluation included the UPDRS, which incorporates assessments of motor function and activities of daily living,23 and a dyskinesia-rating scale.24 The dyskinesia score has a range of 0 (no dyskinesia) to 4 (severe dyskinesia). The double-blind, crossover study was performed after both medication and stimulation had been discontinued overnight. The patients were randomly assigned to undergo motor assessments in one of two treatment sequences. In sequence 1, the first evaluation was performed after stimulation had remained off for two additional hours and the second was performed after stimulation had been turned on for two hours; in sequence 2, the order was reversed. The investigators and patients were unaware of whether stimulation had been on or off. Permuted-block randomization was used to ensure uniform assignment of treatments to patients within each participating center and within each target site of implantation.
Unblinded base-line assessments were performed in the off-medication state (after overnight withdrawal of antiparkinsonian medication) and in the on-medication state (when the patient had his or her best response to the morning dose of antiparkinsonian medication). Unblinded postoperative evaluations were performed sequentially in four conditions (off medication, without stimulation; off medication, with stimulation; on medication, without stimulation; on medication, with stimulation). Evaluations with stimulation were performed after the stimulator had been turned on for approximately 30 minutes. Within each center, all assessments were performed by the same investigator.
The patients completed a home diary documenting their motor status at 30-minute intervals during the two days before each visit. Before the beginning of the study, they were instructed in the identification of three motor states: poor mobility (“off”), good mobility without dyskinesia (“on” without dyskinesia), and good mobility with dyskinesia (“on” with dyskinesia). At the completion of the study, the patients and investigators assessed the global effect of therapy.
Statistical Analysis
The primary outcome measure was the difference between scores on the motor subscale of the UPDRS performed with or without stimulation in the double-blind crossover component of the study. The Wilcoxon rank-sum test25 was used to assess treatment, period, and carryover effects. The analysis of carryover effects assessed whether the treatment intervention in the first evaluation influenced the results obtained in the second. The analysis of the period effect assessed whether there was a difference in the results of stimulation in the two sequences. Secondary end points included the effect of stimulation on the change between base line and six months in the UPDRS motor score in the off-medication and on-medication states; the number of hours per day during which patients had good mobility without dyskinesia; scores on subscales of the UPDRS (activities of daily living, tremor, rigidity, bradykinesia, gait, and postural stability), and levodopa dose equivalents.
The Wilcoxon signed-rank test25 was used for paired comparisons. Repeated-measures analysis of variance25 was used to predict motor scores on the basis of three independent variables: stimulation status, medication status, and time. Analysis of the primary end point was performed for all randomized patients. All data collected at follow-up visits were used in the analysis of secondary end points. All enrolled patients were included in the analysis of adverse events. All P values were two-tailed. No interim analyses were performed.
Medtronic sponsored the study and was responsible for data collection, monitoring, and statistical analysis. The company had no role in study design, interpretation of data, or preparation of the manuscript for publication.
Results
The study was conducted at 18 centers between July 1995 and July 1999. A total of 143 patients were enrolled; 134 received bilateral implants in the subthalamic nucleus or the pars interna of the globus pallidus and were included in the efficacy analysis. Nine patients did not receive bilateral implants. Table 1Table 1
Base-Line Characteristics of the 134 Patients with Bilateral Implants and Stimulation Settings at the Last Follow-up Visit. shows the characteristics of the patients at base line. Bilateral procedures were performed in a single session in 87.5 percent of patients with subthalamic implants and 68.4 percent of those with pallidal implants. Table 1 also shows the stimulation settings at the time of the last visit.Deep-Brain Stimulation of the Subthalamic Nucleus
One hundred two patients were enrolled in the subthalamic-nucleus group. Electrodes were bilaterally implanted in 96 patients, and 91 participated in the double-blind crossover evaluation and completed six months of follow-up. Bilateral procedures were not performed in six patients because of complications of the first surgical procedure (intracranial hemorrhage in two, hemiparesis in one, confusion in one, lack of response in one, and improper lead placement in one). Five did not participate in the double-blind evaluation or the six-month follow-up evaluation (two patients had infected leads, and three withdrew consent).
In the double-blind crossover study, there was a significant treatment effect associated with stimulation (P<0.001) (Table 2Table 2
UPDRS Motor Scores for the Randomized, Double-Blind Crossover Study.); there were no significant carryover effects (P=0.38) or period effects (P=0.47). Thus, stimulation in the first evaluation did not influence the results obtained in the evaluation without stimulation. In addition, stimulation produced the same result regardless of the order in which the patients were evaluated. Stimulation was associated with a mean improvement of 43 percent and a median improvement of 49 percent in the UPDRS motor score in comparison with the evaluation performed without stimulation (P<0.001). Significant benefits were also observed with stimulation in both sequences. A median improvement of more than 25 percent was noted at 15 of the 16 centers that performed this procedure.The results of the unblinded evaluations are provided in Table 3Table 3
Effect of Stimulation and Medication on UPDRS Motor Scores at Unblinded Evaluations.. In comparison with base line, stimulation in the off-medication state was associated with significant improvement in the UPDRS motor score at each visit. Smaller, but significant, benefits were also noted with stimulation in the on-medication state. Stimulation status was significantly associated with the motor score in a repeated-measures analysis of variance (P<0.001). Significant interaction effects between medication and stimulation were observed, suggesting that stimulation and medication act synergistically in predicting motor scores. Follow-up visits did not predict motor score (P=0.58), indicating that the beneficial effect of stimulation was stable over time.Stimulation in the off-medication state was also associated with significant improvement in tremor, rigidity, bradykinesia, gait, postural stability, and activities of daily living (Table 4Table 4
Effect of Subthalamic and Pallidal Stimulation on UPDRS Subscores.). Home-diary assessments of the percentage of time with good mobility and without dyskinesia during the waking day increased from 27 percent to 74 percent between base line and six months (P<0.001); this was paralleled by a decrease in the percentage of time with poor mobility, from 49 percent to 19 percent (P<0.001) (Figure 1Figure 1The Mean Percentage of Time during Waking Hours with Poor Mobility (the “Off” State), Good Mobility with Dyskinesia (the “On” State with Dyskinesia), and Good Mobility without Dyskinesia (the “On” State without Dyskinesia) at Base Line and Six Months after the Implantation of Electrodes for Bilateral Stimulation of Either the Subthalamic Nucleus or the Pars Interna of the Globus Pallidus.). The mean (±SD) dyskinesia score improved from 1.9±1.1 at base line to 0.8±0.8 at six months (P<0.001). Global assessments by physicians and patients noted severe disability at base line in 74 percent and 77 percent, respectively, as compared with 15 percent and 23 percent at six months. Daily levodopa dose equivalents were reduced from a mean of 1218.8±575 mg at base line to 764.0±507 mg at six months (P<0.001).Deep-Brain Stimulation of the Pars Interna of the Globus Pallidus
Forty-one patients were enrolled; electrodes were bilaterally implanted in 38 patients, 35 participated in the double-blind evaluation, and 36 completed six months of follow-up. Bilateral procedures were not performed in three patients because of cerebral hemorrhage in two and intraoperative confusion in one. Three patients did not participate in the double-blind evaluation (two refused, and one withdrew from the study). Two did not complete six months of follow-up (one withdrew, and one died).
The double-blind crossover evaluation performed at three months demonstrated a significant treatment effect in favor of stimulation (P<0.001) (Table 2). There were no significant carryover effects (P=0.40) or period effects (P=0.50). Stimulation was associated with a mean improvement of 32 percent and a median improvement of 37 percent in the UPDRS motor score (P<0.001). Median improvement greater than 25 percent was observed at 9 of 10 centers. The benefit of stimulation was seen regardless of the sequence assignment.
The results of the unblinded evaluations over the course of the study are provided in Table 3. In comparison with base line, there was significant improvement in the UPDRS motor score at each visit with stimulation in the off-medication state (P<0.001). Smaller, but significant, benefits were also noted with stimulation in the on-medication state (P=0.003). Repeated-measures analysis of variance demonstrated that stimulation was significantly associated with improvement in the motor score (P<0.001). An interaction effect between medication and stimulation was observed (P<0.001), and the beneficial effect of stimulation was stable over time (P=0.72).
The effects of pallidal stimulation on activities of daily living and the cardinal features of Parkinson's disease are shown in Table 4. Significant benefits were observed, particularly in the off-medication state. Home-diary assessments indicated that between base line and six months, the percentage of time with good mobility and without dyskinesia during the waking day increased from 28 percent to 64 percent (P<0.001); the percentage of time with poor mobility was correspondingly reduced from 37 percent to 24 percent (P=0.01) (Figure 1). The dyskinesia score improved from a mean of 2.1±1.5 at base line to 0.7±0.8 at six months (P<0.01). Physician and patient global estimates of severe disability improved from 76 percent and 82 percent, respectively, at base line to 11 percent and 14 percent at six months. The mean daily dose in levodopa equivalents was unchanged between base line (1090.9±543 mg) and six months (1120±537 mg).
Adverse Events
All serious or severe adverse events attributed to the intervention or affecting more than one patient are listed in Table 5Table 5
Adverse Events Associated with Subthalamic and Pallidal Stimulation.. Intracranial hemorrhage occurred in seven patients (subcortical in five, subarachnoid in one, and within the subthalamic nucleus in one), four of whom required surgical decompression. Six patients had neurologic deficits associated with the hemorrhage, and four of these had persistent dysfunction (including hemiparesis, aphasia, and cognitive dysfunction). The number of microelectrode passes used to determine target location correlated with the risk of hemorrhage. Patients without hemorrhage had a mean of 2.9±1.8 passes, as compared with 4.1±2.0 among those who had hemorrhage (P=0.05). Four patients had seizures, two of which occurred in patients who had a cerebral hemorrhage. In all instances, seizures were able to be controlled with anticonvulsant medication. The device was explanted because of infection in two patients. Stimulation was frequently associated with muscle twitch and paresthesia, but these were typically transient and disappeared with adjustment of the stimulator settings. Five patients had stimulation-induced dyskinesia; in one patient the dyskinesia was severe but resolved with stimulator adjustment. One patient died of esophageal carcinoma.Discussion
We conducted a six-month, multicenter study of patients with advanced Parkinson's disease who underwent bilateral deep-brain stimulation of the subthalamic nucleus or the pars interna of the globus pallidus. A double-blind, crossover evaluation demonstrated that stimulation of either target improved motor function in the off-medication state. Although initiation of stimulation was associated with transient symptoms in some patients, we do not believe that this influenced the blinded assessment, since neither the patients nor the investigators were certain of whether stimulation was being given at the time.
Unblinded evaluations showed that both subthalamic stimulation and pallidal stimulation were associated with improvement in motor score in the off-medication state. Benefits were observed with respect to total motor score, dyskinesia, activities of daily living, and each of the cardinal features of Parkinson's disease. Home-diary assessments indicated that patients in both groups had a significant increase in the percentage of “on” time without dyskinesia and a significant decrease in the percentage of “off” time. Furthermore, with stimulation, UPDRS motor scores during “off” periods were significantly improved and approximated motor scores during “on” periods induced by medical therapy. Thus, “off” periods were reduced in both frequency and severity, with the result that disability was markedly attenuated. This decrease was reflected in the global evaluation scores of both physicians and patients.
Stimulation in the on-medication state resulted in less pronounced but still significant clinical improvement, suggesting the possibility of synergism between subthalamic or pallidal stimulation and dopaminergic drugs. Such an effect has not been reported with other surgical therapies.11,12,26,27 Dyskinesias were reduced in both groups. A reduction in levodopa dose equivalents may have contributed to this effect in patients treated with stimulation of the subthalamic nucleus. However, this would not account for the reduction in dyskinesia in patients who were receiving pallidal stimulation and in whom the levodopa dose equivalent was not reduced. Alternatively, high-frequency stimulation might have disrupted abnormal neuronal firing patterns in the subthalamic nucleus or the pars interna of the globus pallidus that are responsible for dyskinesia.28 Our results are similar to those reported in other trials of subthalamic18,19 and pallidal20-22 stimulation that involved smaller numbers of patients.
There were seven cases of intracranial hemorrhage in 143 patients who underwent 277 stereotactic procedures. Two patients had infections necessitating removal of the electrodes. The remainder of the complications did not lead to serious morbidity or death. Four patients had persistent neurologic deficits (2.8 percent of patients and 1.4 percent of surgical procedures). This rate is less than that reported with other bilateral surgical procedures for Parkinson's disease.11,13,29-31 There is controversy as to whether the benefit of microelectrode recordings used to facilitate target localization is offset by the risk of additional adverse events.26,32,33 Our study suggests that increased numbers of microelectrode passes were associated with an increased risk of intracranial bleeding.
The mechanism of action of deep-brain stimulation remains to be defined.34 Possible mechanisms include depolarization blockade, release of local inhibitory neurotransmitters, antidromic activation of inhibitory neurons, and jamming of abnormal neuronal firing patterns. By whatever mechanism, stimulation mirrors the effects of a destructive lesion.
In conclusion, bilateral stimulation of the subthalamic nucleus or pars interna of the globus pallidus provides significant motor benefits for patients with advanced Parkinson's disease, while reducing dyskinesia and motor fluctuations. Although we did not conduct a direct comparison, these benefits are of greater magnitude than has been achieved with thalamotomy,31 unilateral pallidotomy,11,12,30,35 thalamic stimulation,17,36 or fetal nigral transplantation.37,38 Serious adverse events appear to be less frequent with bilateral stimulation than with bilateral ablative procedures.13,31 Patients were not randomly assigned to a target site of implantation, and the study was therefore not designed to compare subthalamic and pallidal stimulation. Nonetheless, subthalamic stimulation appears to be associated with a greater benefit and permitted a reduction in the consumption of levodopa or its equivalents. These observations suggest that stimulation of the subthalamic nucleus might be superior to pallidal stimulation, but further studies are required to determine whether one target is preferable to the other.
Supported by a grant from Medtronic Corporation, Minneapolis. Drs. Obeso, Olanow, and Lang, members of the writing committee, have served as paid consultants to Medtronic. Dr. Lang has received additional payments from Medtronic to support a neurology fellowship.
The preparation of this article was overseen by the writing committee (J.A. Obeso, M.D., C.W. Olanow, M.D., M.C. Rodriguez-Oroz, M.D., P. Krack, M.D., R. Kumar, M.D., and A.E. Lang, M.D.), who assume responsibility for the overall content and integrity of the manuscript.
Source Information
Address reprint requests to Dr. Jose A. Obeso at Neurologia–Neurosciencias, Clinica Universitaria, Avenida Pio XII-36, Pamplona 31008, Spain, or at jobeso@unav.es; or to Dr. C.W. Olanow at the Department of Neurology, Box 1137, Mount Sinai School of Medicine, 1 Gustave L. Levy Place, New York, NY 10029, or at warren.olanow@mssm.edu.
The members of the Deep-Brain Stimulation for Parkinson's Disease Study Group are listed in the Appendix.
Appendix
The following investigators were members of the Deep-Brain Stimulation for Parkinson's Disease Study Group: J.A. Obeso, J. Guridi, and M.C. Rodriguez-Oroz (Clinica Quiron, San Sebastian, Spain); Y. Agid, P. Bejjani, and A.M. Bonnet (Groupe Hospitalier Pitié-Salpêtrière, Paris); A.E. Lang, A.M. Lozano, and R. Kumar (Toronto Western Hospital, Toronto); A. Benabid, P. Pollak, and P. Krack (Clinique Neurologique, Grenoble, France); S. Rehncrona, R. Ekberg, and M. Grabowski (University Hospital, Lund, Sweden); A. Albanese, M. Scerrati, and E. Moro (Università Cattolica, Rome); W. Koller, S.B. Wilkinson, and R. Pahwa (University of Kansas Medical Center, Kansas City); J. Volkmann, N. Allert, and H.-J. Freund (Medizinische Einrichtungen der Heinrich Heine Universität, Düsseldorf, Germany); J. Kulisevsky, A. Gironell, and J. Molet (Hospital Santa Cruz y San Pablo, Barcelona, Spain); V. Tronnier, W. Fogel, and M. Krause (Klinikum der Ruprecht-Karls Universität, Heidelberg, Germany); T. Funk, C. Kern, and U. Kestenbach (Universitätsklinikum Benjamin Franklin, Berlin, Germany); R. Iansek, J. Rosenfeld, and A. Churchyard (Victoria Royal Melbourne Hospital, Parkville, Australia); D. O'Sullivan, M. Pell, and R. Markus (St. Vincent's Hospital, Darlinghurst, Australia); A. Bayes, R. Blesa, and B. Oliver (Centro Medico Tecknon, Barcelona, Spain); C.W. Olanow, I.M. Germano, and M. Brin (Mount Sinai Medical Center, New York); J. Jankovic, R.G. Grossman, and W.G. Ondo (Baylor College of Medicine, Houston); J.L. Vitek, R.A.E. Bakay, and M.R. DeLong (Emory School of Medicine, Atlanta); E. Tolosa, J. Rumia, and F. Valldeoriola (Hospital Clinico, Barcelona, Spain); Scientific Committee: A. Benabid, A. Albanese, M.R. DeLong, A.M. Lang, A. Lozano, J.A. Obeso, C.W. Olanow, P. Pollak, W.C. Koller, J. Vitek, and S. Wilkinson.
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Citing Articles
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Gail D. Baura. 2012. Deep Brain Stimulators. , 297-314.
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Fabian J. David, Miriam R. Rafferty, Julie A. Robichaud, Janey Prodoehl, Wendy M. Kohrt, David E. Vaillancourt, Daniel M. Corcos. (2012) Progressive Resistance Exercise and Parkinson's Disease: A Review of Potential Mechanisms. Parkinson's Disease 2012, 1-10
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Saifur Rashid, Gerald Pho, Michael Czigler, Mary A. Werz, Dominique M. Durand. (2012) Low frequency stimulation of ventral hippocampal commissures reduces seizures in a rat model of chronic temporal lobe epilepsy. Epilepsia 53:1, 147-156
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Michael S Okun, Bruno V Gallo, George Mandybur, Jonathan Jagid, Kelly D Foote, Fredy J Revilla, Ron Alterman, Joseph Jankovic, Richard Simpson, Fred Junn, Leo Verhagen, Jeff E Arle, Blair Ford, Robert R Goodman, R Malcolm Stewart, Stacy Horn, Gordon H Baltuch, Brian H Kopell, Frederick Marshall, DeLea Peichel, Rajesh Pahwa, Kelly E Lyons, Alexander I Tröster, Jerrold L Vitek, Michele Tagliati. (2012) Subthalamic deep brain stimulation with a constant-current device in Parkinson's disease: an open-label randomised controlled trial. The Lancet Neurology
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A.W. Quinkert, D.W. Pfaff. (2012) Temporal patterns of deep brain stimulation generated with a true random number generator and the logistic equation: effects on CNS arousal in mice. Behavioural Brain Research
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Juergen Ralf Schlaier, Christine Habermeyer, Jan Warnat, Max Lange, Annette Janzen, Andreas Hochreiter, Martin Proescholdt, Alexander Brawanski, Claudia Fellner. (2011) Discrepancies between the MRI- and the electrophysiologically defined subthalamic nucleus. Acta Neurochirurgica 153:12, 2307-2318
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Ellen L. Air, Jill L. Ostrem, Terence D. Sanger, Philip A. Starr. (2011) Deep brain stimulation in children: experience and technical pearls. Journal of Neurosurgery: Pediatrics 8:6, 566-574
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Meaghan C. Creed, Clement Hamani, José N. Nobrega. (2011) Early gene mapping after deep brain stimulation in a rat model of tardive dyskinesia: Comparison with transient local inactivation. European Neuropsychopharmacology
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Olivia O. Huston, Robert E. Watson, Matt A. Bernstein, Kiaran P. McGee, S. Matt Stead, Debb A. Gorman, Kendall H. Lee, John Huston. (2011) Intraoperative magnetic resonance imaging findings during deep brain stimulation surgery. Journal of Neurosurgery 115:4, 852-857
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Ted Eller. (2011) Deep Brain Stimulation for Parkinson's Disease, Essential Tremor, and Dystonia. Disease-a-Month 57:10, 638-646
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Ali Nabi, Jeff Moehlis. (2011) Single input optimal control for globally coupled neuron networks. Journal of Neural Engineering 8:6, 065008
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E. Trachani, C. Constantoyannis, G. C. Sakellaropoulos, M. L. Stavrinou, G. Nikiforidis, E. Chroni. (2011) Heart rate variability in Parkinson’s disease unaffected by deep brain stimulation. Acta Neurologica Scandinavicano-no
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Robin Bhatia, Arthur Dalton, Mike Richards, Chris Hopkins, Tipu Aziz, Dipankar Nandi. (2011) The incidence of deep brain stimulator hardware infection: the effect of change in antibiotic prophylaxis regimen and review of the literature. British Journal of Neurosurgery 25:5, 625-631
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Fabian Klostermann, Lea Krugel, Michael Wahl. (2011) Learning about language and speech from Deep Brain Stimulation. Journal of Neurolinguistics
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Hideki Oshima, Yoichi Katayama, Takashi Morishita, Koichiro Sumi, Toshiharu Otaka, Kazutaka Kobayashi, Yutaka Suzuki, Chikashi Fukaya, Takamitsu Yamamoto. (2011) Subthalamic nucleus stimulation for attenuation of pain related to Parkinson disease. Journal of Neurosurgery1-8
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Ludvic Zrinzo, Thomas Foltynie, Patricia Limousin, Marwan I. Hariz. (2011) Reducing hemorrhagic complications in functional neurosurgery: a large case series and systematic literature review. Journal of Neurosurgery1-11
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V. G. H. Evidente, A. P. Premkumar, C. H. Adler, J. N. Caviness, E. Driver-Dunckley, M. K. Lyons. (2011) Medication dose reductions after pallidal versus subthalamic stimulation in patients with Parkinson’s disease. Acta Neurologica Scandinavica 124:3, 211-214
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R. Constantinescu, B. Holmberg, L. Rosengren, O. Corneliusson, B. Johnels, H. Zetterberg. (2011) Light subunit of neurofilament triplet protein in the cerebrospinal fluid after subthalamic nucleus stimulation for Parkinson’s disease. Acta Neurologica Scandinavica 124:3, 206-210
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Jennifer Witt, William J. Marks. (2011) An Update on Gene Therapy in Parkinson’s Disease. Current Neurology and Neuroscience Reports 11:4, 362-370
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Elan D. Louis, Michael S. Okun. (2011) It is time to remove the ‘benign’ from the essential tremor label. Parkinsonism & Related Disorders 17:7, 516-520
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Yakov Gologorsky, Sharona Ben-Haim, Erin L Moshier, James Godbold, Michele Tagliati, Donald Weisz, Ron L Alterman. (2011) Transgressing the Ventricular Wall During Subthalamic Deep Brain Stimulation Surgery for Parkinson Disease Increases the Risk of Adverse Neurological Sequelae. Neurosurgery 69:2, 294-300
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Jin Hoon Park, Sun Ju Chung, Chong Sik Lee, Sang Ryong Jeon. (2011) Analysis of hemorrhagic risk factors during deep brain stimulation surgery for movement disorders: comparison of the circumferential paired and multiple electrode insertion methods. Acta Neurochirurgica 153:8, 1573-1578
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C. Warren Olanow, Fabrizio Stocchi, Anthony E. Lang. 2011. The Dopaminergic and Non-Dopaminergic Features of Parkinson's Disease. , 1-6.
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Shearwood McClelland. (2011) A cost analysis of intraoperative microelectrode recording during subthalamic stimulation for Parkinson's disease. Movement Disorders 26:8, 1422-1427
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José Fidel Baizabal Carvallo, Richard Simpson, Joseph Jankovic. (2011) Diagnosis and treatment of complications related to deep brain stimulation hardware. Movement Disorders 26:8, 1398-1406
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Marwan I. Hariz. (2011) Surgical probings into the basal ganglia: Hemorrhage and hardware-related risks, and costs of microelectrode recording. Movement Disorders 26:8, 1375-1377
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Rüdiger Hilker, Angelo Antonini, Per Odin. (2011) What is the best treatment for fluctuating Parkinson’s disease: continuous drug delivery or deep brain stimulation of the subthalamic nucleus?. Journal of Neural Transmission 118:6, 907-914
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Thomas Mera, Jerrold L. Vitek, Jay L. Alberts, Joseph P. Giuffrida. (2011) Kinematic optimization of deep brain stimulation across multiple motor symptoms in Parkinson's disease. Journal of Neuroscience Methods 198:2, 280-286
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Matthew J. Tormenti, Nestor D. Tomycz, Keith A. Coffman, Douglas Kondziolka, Donald J. Crammond, Elizabeth C. Tyler-Kabara. (2011) Bilateral subthalamic nucleus deep brain stimulation for dopa-responsive dystonia in a 6-year-old child. Journal of Neurosurgery: Pediatrics 7:6, 650-653
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A. E. Elia, C. Dollenz, P. Soliveri, A. Albanese. (2011) Motor features and response to oral levodopa in patients with Parkinson’s disease under continuous dopaminergic infusion or deep brain stimulation. European Journal of Neurologyno-no
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Ashutosh Chaturvedi, Thomas J. Foutz, Cameron C. McIntyre. (2011) Current steering to activate targeted neural pathways during deep brain stimulation of the subthalamic region. Brain Stimulation
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Han-Joon Kim, Beom S Jeon, Jee-Young Lee, Sun Ha Paek, Dong Gyu Kim. (2011) The benefit of subthalamic deep brain stimulation on pain in Parkinson disease: a 2-year follow-up study. Neurosurgery1
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C. Warren Olanow, Kathryn B. Wunderle, Karl Kieburtz. (2011) Milestones in movement disorders clinical trials: Advances and landmark studies. Movement Disorders 26:6, 1003-1014
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Sharon Norman, Ravi Bellamkonda. 2011. MEMS in the Nervous System. .
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Gun-Marie Hariz, Takeshi Nakajima, Patricia Limousin, Tom Foltynie, Ludvic Zrinzo, Marjan Jahanshahi, Katarina Hamberg. (2011) Gender distribution of patients with Parkinson’s disease treated with subthalamic deep brain stimulation; a review of the 2000–2009 literature. Parkinsonism & Related Disorders 17:3, 146-149
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Karsten Witt, Jens Kuhn, Lars Timmermann, Mateusz Zurowski, Christiane Woopen. (2011) Deep Brain Stimulation and the Search for Identity. Neuroethics
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Christopher R. Butson, Scott E. Cooper, Jaimie M. Henderson, Barbara Wolgamuth, Cameron C. McIntyre. (2011) Probabilistic analysis of activation volumes generated during deep brain stimulation. NeuroImage 54:3, 2096-2104
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Roberto Cilia, Sang Soo Cho, Thilo van Eimeren, Giorgio Marotta, Chiara Siri, Ji Hyun Ko, Giovanna Pellecchia, Gianni Pezzoli, Angelo Antonini, Antonio P. Strafella. (2011) Pathological gambling in patients with Parkinson's disease is associated with fronto-striatal disconnection: A path modeling analysis. Movement Disorders 26:2, 225-233
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Tejas Sankar, Andres M. Lozano. 2011. Surgical Approach to l-Dopa-Induced Dyskinesias. , 151-171.
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Nobuko Kemmotsu, Catherine C. Price, Genko Oyama, Michael S. Okun, Kelly D. Foote, Laura L. S. Howe, Dawn Bowers. (2011) Pre- and Post- GPi DBS Neuropsychological Profiles in a Case of X-Linked Dystonia-Parkinsonism. The Clinical Neuropsychologist 25:1, 141-159
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Gilberto Fisone, Erwan Bezard. 2011. Molecular Mechanisms of l-DOPA-Induced Dyskinesia. , 95-122.
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Paresh K. Doshi. (2011) Long-Term Surgical and Hardware-Related Complications of Deep Brain Stimulation. Stereotactic and Functional Neurosurgery 89:2, 89-95
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Stanley Fahn, Joseph Jankovic, Mark Hallett. 2011. Surgical treatment of Parkinson disease and other movement disorders. , 157-182.
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Atsushi UMEMURA, Yuichi OKA, Kenichi YAMAMOTO, Kenji OKITA, Noriyuki MATSUKAWA, Kazuo YAMADA. (2011) Complications of Subthalamic Nucleus Stimulation in Parkinson's Disease. Neurologia medico-chirurgica 51:11, 749-755
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Fabian Klostermann, Michael Wahl, Frank Marzinzik, Jan Vesper, Werner Sommer, Gabriel Curio. (2010) Speed effects of deep brain stimulation for Parkinson's disease. Movement Disorders 25:16, 2762-2768
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Efstathios J. Boviatsis, Lampis C. Stavrinou, Marios Themistocleous, Andreas T. Kouyialis, Damianos E. Sakas. (2010) Surgical and hardware complications of deep brain stimulation. A seven-year experience and review of the literature. Acta Neurochirurgica 152:12, 2053-2062
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Wieslaw L. Nowinski, Beng Choon Chua, Ihar Volkau, Fiftarina Puspitasari, Yevgen Marchenko, Val M. Runge, Michael V. Knopp. (2010) Simulation and assessment of cerebrovascular damage in deep brain stimulation using a stereotactic atlas of vasculature and structure derived from multiple 3- and 7-tesla scans. Journal of Neurosurgery 113:6, 1234-1241
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Jelle Demeestere, Wim Vandenberghe. (2010) Experimental Surgical Therapies for Huntington's Disease. CNS Neuroscience & Therapeuticsno-no
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Claire L. Tomlinson, Rebecca Stowe, Smitaa Patel, Caroline Rick, Richard Gray, Carl E. Clarke. (2010) Systematic review of levodopa dose equivalency reporting in Parkinson's disease. Movement Disorders 25:15, 2649-2653
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Gaia Giannicola, Sara Marceglia, Lorenzo Rossi, Simona Mrakic-Sposta, Paolo Rampini, Filippo Tamma, Filippo Cogiamanian, Sergio Barbieri, Alberto Priori. (2010) The effects of levodopa and ongoing deep brain stimulation on subthalamic beta oscillations in Parkinson's disease. Experimental Neurology 226:1, 120-127
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W. H. Oertel, A. Berardelli, B. R. Bloem, U. Bonuccelli, D. Burn, G. Deuschl, E. Dietrichs, G. Fabbrini, J. J. Ferreira, A. Friedman, P. Kanovsky, V. Kostic, A. Nieuwboer, P. Odin, W. Poewe, O. Rascol, C. Sampaio, M. Schüpbach, E. Tolosa, C. Trenkwalder. 2010. Late (Complicated) Parkinson's Disease. , 237-267.
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Marvin A. Rossi, Glenn Stebbins, Christopher Murphy, David Greene, Spencer Brinker, David Sarcu, Aaron Tenharmsel, Travis Stoub, Michael A. Stein, Thomas J. Hoeppner, Richard W. Byrne, Michael E. Moseley, Roland A. Bammer, Steve Bild, Jennifer Dennis, Nichole Arnett, Antoaneta Balabanov, Donna Bergen, Andres M. Kanner, Michael C. Smith. (2010) Predicting white matter targets for direct neurostimulation therapy. Epilepsy Research 91:2-3, 176-186
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Harrison N. Jones, Diane L. Kendall, Michael S. Okun, Samuel S. Wu, Craig Velozo, Hubert H. Fernandez, Kristie A. Spencer, John C. Rosenbek. (2010) Speech motor program maintenance, but not switching, is enhanced by left-hemispheric deep brain stimulation in Parkinson's disease. International Journal of Speech-Language Pathology 12:5, 385-398
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Ricardo J Komotar, Robert M Starke, E Sander Connolly, Robert R Goodman. (2010) Pallidal Vs Subthalamic Deep Brain Stimulation for Parkinson Disease. Neurosurgery 67:4, N25-N27
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Young Seok Park, Hae Yoo Kim, Won Seok Chang, Phil Hyu Lee, Young Ho Sohn, Jin Woo Chang. (2010) A Comparison of LEDD and Motor Scores Following STN-DBS Treatment in Patient with Young Onset vs. Late Onset Parkinson's Disease. Neuromodulation: Technology at the Neural Interface 13:4, 255-260
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Elizabeth A. M. Frost, Irene Osborn. (2010) Deep Brain Stimulation—Surgery for Movement Disorders and Parkinsonʼs Disease. International Anesthesiology Clinics 47:2, 57-68
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Zang-Hee Cho, Hoon-Ki Min, Se-Hong Oh, Jae-Yong Han, Chan-Woong Park, Je-Geun Chi, Young-Bo Kim, Sun Ha Paek, Andres M. Lozano, Kendall H. Lee. (2010) Direct visualization of deep brain stimulation targets in Parkinson disease with the use of 7-tesla magnetic resonance imaging. Journal of Neurosurgery 113:3, 639-647
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Molly M. Sturman, David E. Vaillancourt, Leo Verhagen Metman, Roy A. E. Bakay, Daniel M. Corcos. (2010) Effects of five years of chronic STN stimulation on muscle strength and movement speed. Experimental Brain Research 205:4, 435-443
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Jared M. Pisapia, Casey H. Halpern, Noel N. Williams, Thomas A. Wadden, Gordon H. Baltuch, Sherman C. Stein. (2010) Deep brain stimulation compared with bariatric surgery for the treatment of morbid obesity: a decision analysis study. Neurosurgical FOCUS 29:2, E15
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Dunbar Alcindor, Michael Y. Oh, Susan Baser, Cindy Angle, Boyle C. Cheng, Donald Whiting. (2010) Stimulation of the globus pallidus internus in a patient with DYT1-positive primary generalized dystonia: a 10-year follow-up. Neurosurgical FOCUS 29:2, E16
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Vivianne L. Tawfik, Su-Youne Chang, Frederick L. Hitti, David W. Roberts, James C. Leiter, Svetlana Jovanovic, Kendall H. Lee. (2010) Deep Brain Stimulation Results in Local Glutamate and Adenosine Release. Neurosurgery 67:2, 367-375
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Roberto Cilia, Ji Hyun Ko, Sang Soo Cho, Thilo van Eimeren, Giorgio Marotta, Giovanna Pellecchia, Gianni Pezzoli, Angelo Antonini, Antonio P. Strafella. (2010) Reduced dopamine transporter density in the ventral striatum of patients with Parkinson's disease and pathological gambling. Neurobiology of Disease 39:1, 98-104
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J. Voges, J.K. Krauss. (2010) Neurochirurgische und technische Aspekte der tiefen Hirnstimulation. Der Nervenarzt 81:6, 702-710
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M J Lehmkuhle, S M Mayes, D R Kipke. (2010) Unilateral neuromodulation of the ventromedial hypothalamus of the rat through deep brain stimulation. Journal of Neural Engineering 7:3, 036006
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Thomas Foltynie, Marwan I Hariz. (2010) Surgical management of Parkinson’s disease. Expert Review of Neurotherapeutics 10:6, 903-914
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Kelly L. Collins, Emily M. Lehmann, Parag G. Patil. (2010) Deep brain stimulation for movement disorders. Neurobiology of Disease 38:3, 338-345
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Hisayoshi Oka, Chizuko Toyoda, Makiko Yogo, Soichiro Mochio. (2010) Olfactory dysfunction and cardiovascular dysautonomia in Parkinson’s disease. Journal of Neurology 257:6, 969-976
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Toru Yasuda, Hideki Mochizuki. (2010) Use of growth factors for the treatment of Parkinson’s disease. Expert Review of Neurotherapeutics 10:6, 915-924
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Christopher Janson, Robert Maxwell, Akshay A. Gupte, Aviva Abosch. (2010) Bowstringing as a Complication of Deep Brain Stimulation. Neurosurgery 66:6, E1205
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E. L. Johnsen, N. Sunde, P. H. Mogensen, K. Østergaard. (2010) MRI verified STN stimulation site - gait improvement and clinical outcome. European Journal of Neurology 17:5, 746-753
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Elena Moro, Andres M. Lozano, Pierre Pollak, Yves Agid, Stig Rehncrona, Jens Volkmann, Jaime Kulisevsky, Jose A. Obeso, Alberto Albanese, Marwan I. Hariz, Niall P. Quinn, Jans D. Speelman, Alim L. Benabid, Valerie Fraix, Alexandre Mendes, Marie-Laure Welter, Jean-Luc Houeto, Philippe Cornu, Didier Dormont, Annalena L. Tornqvist, Ron Ekberg, Alfons Schnitzler, Lars Timmermann, Lars Wojtecki, Andres Gironell, Maria C. Rodriguez-Oroz, Jorge Guridi, Anna R. Bentivoglio, Maria F. Contarino, Luigi Romito, Massimo Scerrati, Marc Janssens, Anthony E. Lang. (2010) Long-term results of a multicenter study on subthalamic and pallidal stimulation in Parkinson's disease. Movement Disorders 25:5, 578-586
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C. Rossi, D. Frosini, D. Volterrani, P. De Feo, E. Unti, V. Nicoletti, L. Kiferle, U. Bonuccelli, R. Ceravolo. (2010) Differences in nigro-striatal impairment in clinical variants of early Parkinson’s disease: evidence from a FP-CIT SPECT study. European Journal of Neurology 17:4, 626-630
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Ashutosh Chaturvedi, Christopher R. Butson, Scott F. Lempka, Scott E. Cooper, Cameron C. McIntyre. (2010) Patient-specific models of deep brain stimulation: Influence of field model complexity on neural activation predictions. Brain Stimulation 3:2, 65-77
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Eftichia Trachani, Constantine Constantoyannis, Vassiliki Sirrou, Zinovia Kefalopoulou, Elli Markaki, Elisabeth Chroni. (2010) Effects of subthalamic nucleus deep brain stimulation on sweating function in Parkinson's disease. Clinical Neurology and Neurosurgery 112:3, 213-217
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Niels Allert, Ralph Lehrke, Volker Sturm, Jens Volkmann. (2010) Secondary failure after ten years of pallidal neurostimulation in a patient with advanced Parkinson’s disease. Journal of Neural Transmission 117:3, 349-351
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Robert Fisher, Vicenta Salanova, Thomas Witt, Robert Worth, Thomas Henry, Robert Gross, Kalarickal Oommen, Ivan Osorio, Jules Nazzaro, Douglas Labar, Michael Kaplitt, Michael Sperling, Evan Sandok, John Neal, Adrian Handforth, John Stern, Antonio DeSalles, Steve Chung, Andrew Shetter, Donna Bergen, Roy Bakay, Jaimie Henderson, Jacqueline French, Gordon Baltuch, William Rosenfeld, Andrew Youkilis, William Marks, Paul Garcia, Nicolas Barbaro, Nathan Fountain, Carl Bazil, Robert Goodman, Guy McKhann, K. Babu Krishnamurthy, Steven Papavassiliou, Charles Epstein, John Pollard, Lisa Tonder, Joan Grebin, Robert Coffey, Nina Graves, . (2010) Electrical stimulation of the anterior nucleus of thalamus for treatment of refractory epilepsy. Epilepsia
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Takashi Morishita, Kelly D. Foote, Samuel S. Wu, Charles E. Jacobson, Ramon L. Rodriguez, Ihtsham U. Haq, Mustafa S. Siddiqui, Irene A. Malaty, Christopher J. Hass, Michael S. Okun. (2010) Brain penetration effects of microelectrodes and deep brain stimulation leads in ventral intermediate nucleus stimulation for essential tremor. Journal of Neurosurgery 112:3, 491-496
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A. M. M. Frankemolle, J. Wu, A. M. Noecker, C. Voelcker-Rehage, J. C. Ho, J. L. Vitek, C. C. McIntyre, J. L. Alberts. (2010) Reversing cognitive-motor impairments in Parkinson's disease patients using a computational modelling approach to deep brain stimulation programming. Brain 133:3, 746-761
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Alessandro Stefani, Mariangela Pierantozzi, Giacomo Koch, Salvatore Galati, Paolo Stanzione. (2010) Therapy for dyskinesias in Parkinson’s disease patients. Future Neurology 5:2, 277-299
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Angelo Antonini, K. Ray Chaudhuri, Pablo Martinez-Martin, Per Odin. (2010) Oral and Infusion Levodopa-Based Strategies for Managing Motor Complications in Patients with Parkinsonʼs Disease. CNS Drugs 24:2, 119-129
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A.M. Lozano. 2010. Surgery for Movement Disorders, Overview, Including History. , 199-200.
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Tiphaine Rouaud, Thibaut Dondaine, Sophie Drapier, Claire Haegelen, François Lallement, Julie Péron, Sylvie Raoul, Paul Sauleau, Marc Vérin. (2010) Pallidal stimulation in advanced Parkinson's patients with contraindications for subthalamic stimulation. Movement Disordersn/a-n/a
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Judith R. Walters, Debra A. Bergstrom. 2010. Synchronous Activity in Basal Ganglia Circuits. , 429-443.
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Florent Lalys, Claire Haegelen, Jean-Christophe Ferre, Omar El-Ganaoui, Pierre Jannin. (2010) Construction and assessment of a 3-T MRI brain template. NeuroImage 49:1, 345-354
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Joseph Sebeo, Stacie G. Deiner, Ron L. Alterman, Irene P. Osborn. (2010) Anesthesia for Pediatric Deep Brain Stimulation. Anesthesiology Research and Practice 2010, 1-4
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B D Greenberg, L A Gabriels, D A Malone, A R Rezai, G M Friehs, M S Okun, N A Shapira, K D Foote, P R Cosyns, C S Kubu, P F Malloy, S P Salloway, J E Giftakis, M T Rise, A G Machado, K B Baker, P H Stypulkowski, W K Goodman, S A Rasmussen, B J Nuttin. (2010) Deep brain stimulation of the ventral internal capsule/ventral striatum for obsessive-compulsive disorder: worldwide experience. Molecular Psychiatry 15:1, 64-79
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Kazumichi Yamada, Tadashi Hamasaki, Jun-ichi Kuratsu. (2009) Subthalamic nucleus stimulation applied in the earlier vs. advanced stage of Parkinson's disease – Retrospective evaluation of postoperative independence in pursuing daily activities. Parkinsonism & Related Disorders 15:10, 746-751
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Santiago Ortiz-Pérez, Bernardo Sánchez-Dalmau, Juan Molina, Alfredo Adán, Santiago Candela, Jordi Rumià. (2009) Ocular Tilt Reaction as a Delayed Complication of Deep Brain Stimulation for Parkinson Disease. Journal of Neuro-Ophthalmology 29:4, 286-288
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Juliana Lockman, Robert S. Fisher. (2009) Therapeutic Brain Stimulation for Epilepsy. Neurologic Clinics 27:4, 1031-1040
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C. Warren Olanow, Jeffrey H. Kordower, Anthony E. Lang, Jose A. Obeso. (2009) Dopaminergic transplantation for parkinson's disease: Current status and future prospects. Annals of Neurology 66:5, 591-596
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Julio C. Gutiérrez, Fernando J. Seijo, Marco A. Álvarez Vega, Fernando Fernández González, Beatriz Lozano Aragoneses, Marta Blázquez. (2009) Therapeutic extradural cortical stimulation for Parkinson's Disease: Report of six cases and review of the literature. Clinical Neurology and Neurosurgery 111:8, 703-707
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Peter Giacobbe, Helen S. Mayberg, Andres M. Lozano. (2009) Treatment resistant depression as a failure of brain homeostatic mechanisms: Implications for deep brain stimulation. Experimental Neurology 219:1, 44-52
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Benzi M. Kluger, Olga Klepitskaya, Michael S. Okun. (2009) Surgical Treatment of Movement Disorders. Neurologic Clinics 27:3, 633-677
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Xu-dong Zhao, Yi-qun Cao, Han-hua Liu, Feng-qian Li, Ben-ming You, Xiao-ping Zhou. (2009) Long term high frequency stimulation of STN increases dopamine in the corpus striatum of hemiparkinsonian rhesus monkey. Brain Research 1286, 230-238
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Laura B. Zahodne, Michael S. Okun, Kelly D. Foote, Hubert H. Fernandez, Ramon L. Rodriguez, Samuel S. Wu, Lindsey Kirsch-Darrow, Charles E. Jacobson, Christian Rosado, Dawn Bowers. (2009) Greater improvement in quality of life following unilateral deep brain stimulation surgery in the globus pallidus as compared to the subthalamic nucleus. Journal of Neurology 256:8, 1321-1329
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Paul Silberstein, Richard G Bittar, Richard Boyle, Raymond Cook, Terry Coyne, Dudley O’Sullivan, Malcolm Pell, Richard Peppard, Julian Rodrigues, Peter Silburn, Rick Stell, Peter Watson. (2009) Deep brain stimulation for Parkinson’s disease: Australian referral guidelines. Journal of Clinical Neuroscience 16:8, 1001-1008
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John S. Pezaris, Emad N. Eskandar. (2009) Getting signals into the brain: visual prosthetics through thalamic microstimulation. Neurosurgical FOCUS 27:1, E6
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Pablo Andrade, José D. Carrillo-Ruiz, Fiacro Jiménez. (2009) A systematic review of the efficacy of globus pallidus stimulation in the treatment of Parkinson’s disease. Journal of Clinical Neuroscience 16:7, 877-881
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Jens Volkmann, Alberto Albanese, Jaime Kulisevsky, Aana-Lena Tornqvist, Jean-Luc Houeto, Bernard Pidoux, Anne-Marie Bonnet, Alexandre Mendes, Alim-Louis Benabid, Valerie Fraix, Nadege Van Blercom, Jing Xie, José Obeso, Maria Cruz Rodriguez-Oroz, Jurge Guridi, Alfons Schnitzler, Lars Timmermann, Alexandre A. Gironell, Juan Molet, Benta Pascual-Sedano, Stig Rehncrona, Elena Moro, Anthony C. Lang, Andres M. Lozano, Anna Rita Bentivoglio, Massimo Scerrati, Maria Fiorella Contarino, Luigi Romito, Marc Janssens, Yves Agid. (2009) Long-term effects of pallidal or subthalamic deep brain stimulation on quality of life in Parkinson's disease. Movement Disorders 24:8, 1154-1161
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