Tejas Sankar, Travis S. Tierney, Clement Hamani
  1. Department of Neurosurgery, Toronto Western Hospital, Toronto, Ontario, Canada

Correspondence Address:
Clement Hamani
Department of Neurosurgery, Toronto Western Hospital, Toronto, Ontario, Canada


Copyright: © 2012 Sankar T. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

How to cite this article: Sankar T, Tierney TS, Hamani C. Novel applications of deep brain stimulation. Surg Neurol Int 14-Jan-2012;3:

How to cite this URL: Sankar T, Tierney TS, Hamani C. Novel applications of deep brain stimulation. Surg Neurol Int 14-Jan-2012;3:. Available from:

Date of Submission

Date of Acceptance

Date of Web Publication


The success of deep brain stimulation (DBS) surgery in treating medically refractory symptoms of some movement disorders has inspired further investigation into a wide variety of other treatment-resistant conditions. These range from disorders of gait, mood, and memory to problems as diverse as obesity, consciousness, and addiction. We review the emerging indications, rationale, and outcomes for some of the most promising new applications of DBS in the treatment of postural instability associated with Parkinson's disease, depression, obsessive–compulsive disorder, obesity, substance abuse, epilepsy, Alzheimer′s-type dementia, and traumatic brain injury. These studies reveal some of the excitement in a field at the edge of a rapidly expanding frontier. Much work still remains to be done on basic mechanism of DBS, optimal target and patient selection, and long-term durability of this technology in treating new indications.

Keywords: Alzheimer's disease, deep brain stimulation, depression, epilepsy, movement disorders, psychiatry


The modern application of deep brain stimulation (DBS) to the treatment of neurological illness began in the late 1980s with the pioneering work of Benabid and colleagues,[ 10 11 ] who successfully treated patients with Parkinsonian and essential tremor by high-frequency electrical stimulation of the thalamus. With its obvious advantages over traditional ablative neurosurgical procedures including reversibility, adjustability, and titratability, DBS quickly established itself as a mainstay of the therapeutic armamentarium in functional neurosurgery. In particular, DBS has proven its safety and efficacy in the management of patients with Parkinson's disease (PD), tremor, and dystonia. While the precise mechanisms of action of DBS are still being elucidated, its unquestioned efficacy in treating movement disorders has stimulated interest in its application to debilitating diseases previously considered outside the realm of neurosurgical intervention. This search for emerging applications of DBS has also been aided by progress in our understanding of the pathophysiological basis of refractory disease in neurology and psychiatry. We review here recent and promising novel applications of DBS reported in preliminary clinical trials.


A number of recent studies have provided convincing evidence that both pallidal (globus pallidus internus or GPi) and subthalamic nucleus (STN) DBS are highly effective in treating PD. DBS improves the cardinal motor symptoms of PD including tremor,[ 13 25 49 ] rigidity,[ 105 113 ] and bradykinesia.[ 19 113 116 ] It is also effective against some of the dose-limiting side effects of prolonged levodopa therapy, namely, motor fluctuations and disabling dykinesias.[ 44 84 ] In fact, there is now class I evidence from large randomized, controlled trials that DBS is superior to the best medical management in patients with moderate to severe PD.[ 24 131 133 ] Unfortunately, advanced PD patients suffer from a large burden of non-motor symptoms which respond poorly both to medication and to DBS at the standard GPi or STN targets. These so-called non-levodopa responsive symptoms can be significant drivers of disability, and include disorders of cognition, mood, olfaction, sleep, gait, and posture.[ 1 102 115 ] Gait impairment and postural instability, in particular, account for considerable morbidity: at 10 years after the initial diagnosis of PD, approximately 50% of patients are falling, and at 20 years, a substantial proportion have sustained a fracture as a direct consequence of their falls.[ 52 ]

As a result, there has been renewed interest in understanding the neuroanatomical substrates of locomotion and their relevance in PD. Early work on decerebrate cats first suggested that electrical stimulation in the brainstem could initiate or enhance locomotive behavior.[ 92 106 ] This work led to the subsequent discovery of a midbrain locomotor region in mammals,[ 37 38 ] a region that would also encompass the pedunculopontine nucleus (PPN).[ 93 ] Several groups have now performed DBS of the PPN region to address the gait and postural disturbances associated with PD.[ 30 81 83 94 96 109 ] Initial reports of efficacy are promising, particularly for the treatment of freezing of gait and falls.[ 83 ] The enthusiasm generated by the early results of PPN DBS must be tempered by several unresolved issues associated with this novel target. For one, it is unknown which neural structures within or around the PPN mediate therapeutic effect, though some evidence has emerged implicating cholinergic neurons within the nucleus in non-human primates.[ 60 ] In addition, the impact of PPN stimulation on functions unrelated to gait, such as sleep and cognition,[ 8 47 69 98 110 111 ] remains to be worked out. Larger controlled trials will be necessary to establish criteria for optimal patient selection as well as the durability of the therapy.


The notion of neurosurgery for psychiatric disorders evokes memories of a troubled past. The misguided and indiscriminant application of lobotomy with its unacceptable rate of morbidity, coupled with the development of effective psychotropic medications nearly led to the demise of psychiatric surgical procedures by the 1960s.[ 134 ] While a few neurosurgical centers have continued to perform stereotactic ablative procedures for patients with intractable psychiatric conditions, it was not until the last decade, with the emergence of DBS as an accepted therapeutic modality, that psychiatric surgery underwent a resurrection. Much of the renewed enthusiasm in the field has recently been focused on using DBS to manage refractory depression.[ 53 ]

Major depressive disorder (MDD) is a prevalent and costly illness. Recent data suggest that it afflicts more than 121 million people worldwide.[ 91 ] By 2020, MDD is projected to become the second leading cause of disease burden worldwide with profound public health consequences.[ 70 ] Despite the availability of several new classes of anti-depressant medications, evidence-based psychotherapy, and electroconvulsive therapy (ECT), relapse is very common.[ 40 ] In all, 10–20% patients respond poorly to the existing therapies and are classified as having treatment-resistant depression (TRD).[ 29 ] For these patients, there is a considerable and urgent need for new and effective treatment options.

DBS is now being used to target nodes within dysregulated mood circuits. Among these, a commonly studied region is the subcallosal cingulate gyrus (SCG). Functional imaging studies demonstrate SCG overactivity in depressed patients, accompanied by corresponding reductions in activity in associated prefrontal and premotor cortical areas (areas 9 and 46).[ 79 80 ] This pattern of activation is reversed in patients successfully treated with antidepressant medications, cognitive behavioral therapy, or ECT.[ 28 41 78 86 ] These findings prompted the conduction of a pilot trial on SCG DBS in TRD patients.[ 80 ] At 6 months following implantation, four of six patients were responders (defined by >50% reduction in the Hamilton Rating Scale for Depression-17) and two patients had achieved remission. Furthermore, positron emission tomography (PET) imaging showed a reversal of SCG overactivity and impaired frontal cortex metabolism. No patients suffered neurological or cognitive side effects attributable to DBS in this pilot study, although two patients ultimately required electrode explantation owing to infection.

Long-term follow-up data from an extended cohort of 20 patients treated with SCG DBS have now been published.[ 61 71 ] At 3–6 years following implantation (mean 3.5 years), the average response rate was 64.3% and the average remission rate was 42.9%. Patients showed considerable improvement in social functioning and in the degree of involvement in work-related activity at last follow-up.[ 61 ] While no unexpected neurocognitive or device-related complications were reported, two patients committed suicide, although these deaths could not be attributed expressly to either stimulation or device failure. In short, all data to date suggest that SCG DBS is safe, effective, and durable in treating patients suffering from TRD.

Several other targets for DBS in depression other than the SCG have now emerged. Preliminary data from pilot studies of bilateral DBS of the ventral caudate/ventral striatum (VC/VS),[ 75 ] nucleus accumbens (NAcc),[ 12 101 ] inferior thalamic peduncle (ITP),[ 57 ] and lateral habenula[ 99 ] show similar efficacy to SCG stimulation. As with the SCG, these alternate targets may effectively be thought of as critical nodes within the neurocircuitry of depression. Currently, there are no head-to-head data establishing the superiority of one target over any other; it remains to be seen if there is in fact a single optimal target in TRD or whether different symptoms lend themselves to different targets.[ 40 ] Proving long-term efficacy will ultimately require rigorous placebo-controlled trials in which antidepressant response is assessed by observers blinded to stimulation status.


Gilles de la Tourette syndrome (TS) is characterized by the childhood onset of intrusive and chronic motor or vocal tics.[ 66 72 ] Though self-limited in most patients, with a significant decline in tic frequency after the age of 20,[ 36 ] DBS has been applied to treatment-resistant cases persisting into adulthood. The first case report of DBS for TS was published in 1999;[ 122 ] the patient was treated with electrodes placed bilaterally in the thalamus, aiming to target intralaminar and the ventral oralis internus nuclei. Since this initial report, several studies have reported efficacy with thalamic,[ 2 4 9 54 73 97 104 ] pallidal,[ 4 22 26 77 ] NAcc,[ 65 ] and anterior limb of the internal capsule (ALIC) stimulation.[ 33 65 ] To date, there have been four small randomized, blind trials of DBS in adult TS which have all reported significant symptom improvement in the on state but no consensus regarding the optimal target.[ 3 54 73 132 ]

Obsessive-compulsive disorder (OCD) is an anxiety disorder in which unwanted and repeated thoughts, feelings, ideas, or sensations (obsessions) result in patients feeling compelled to perform certain repetitive behaviors (compulsions). Functionally disabling in 40% and medically intractable in 10% of sufferers, OCD has long been treated with ablative neurosurgical procedures including cingulotomy and anterior capsulotomy, with some success.[ 27 82 ] Several small series of DBS for OCD have been published in the last decade. Targets have included the ALIC,[ 16 87 90 ] STN,[ 34 ] VC/VS,[ 7 43 ] ITP,[ 58 ] and NAcc.[ 90 ] More recently, randomized, double-blind trials have assessed DBS in the NAcc (bilaterally[ 23 ] and unilaterally[ 55 ] ) ALIC,[ 42 ] and STN.[ 74 ] As with DBS in other psychiatric disorders, the optimal target has yet to be defined, and the response to stimulation has been variable, though promising: as reported in recent reviews, approximately one-third to half of all patients treated to date would be classified as responders, demonstrating at least a 35% reduction in Yale–Brown Obsessive Compulsive Scale (Y-BOCS) scores.[ 21 43 ] Overall, DBS in the setting of OCD has been safe, although unanticipated adverse neuropsychiatric effects due to stimulation, such as mania, have been reported.[ 48 ]

The well-established importance of dopamine release in the NAcc to the reward system of the brain[ 56 ] has stimulated interest in applying DBS at this target to control addiction. Preliminary reports on the experience with this application are now emerging. Kuhn et al.[ 64 ] treated a 54-year-old patient with agoraphobia, panic attacks, depression, and comorbid alcohol dependency with bilateral NAcc DBS. Although the patient exhibited only a slight improvement in anxiety and depression at 1 year, there was a dramatic and sustained reduction in alcohol consumption. Since this initial report, Muller et al.[ 85 ] have published their clinical experience with NAcc DBS in three patients with chronic resistant alcoholism, reporting a sustained reduction in alcohol cravings, as well as complete alcohol abstinence in two patients and a marked reduction in intake in the third, following one full year of chronic DBS. Zhou et al.[ 138 ] recently published a case report of a 24 year-old man suffering from heroin dependence in whom bilateral, high-frequency stimulation of the NAcc was employed, producing an immediate and complete abstinence from drug use and opioid-seeking behavior. The patient remained relapse-free at 6 years of follow-up, despite stimulation having been permanently discontinued 2½ years after DBS implantation. He also experienced a dramatic decrease in smoking behavior. Similarly, Mantione et al.[ 76 ] described a patient treated with NAcc DBS for OCD in whom postoperative unintended and effortless smoking cessation was observed. The patient also experienced weight loss; indeed NAcc stimulation has also been suggested as a potential target for the treatment of morbid obesity, given that modulation of reward sensations may affect dietary preferences.[ 45 72 ] However, preliminary attempts to use DBS in obesity have mainly targeted the lateral and ventromedial hypothalamic regions corresponding to the appetite and satiety centers of the brain, with some evidence of effect on food intake but unconvincing results with respect to actual weight loss.[ 45 95 117 ] No doubt DBS will have to prove its worth compared to standard therapies for addiction and obesity.


It is estimated that 1% of all adults suffer from epilepsy, with close to 30% of cases being refractory to conventional antiepileptic therapy.[ 50 51 ] While carefully selected patients may benefit from resective surgical procedures, a large number are not candidates for surgery and there is a definite need for effective treatment alternatives. Neuromodulatory procedures for epilepsy have long attempted to fill that void and predate the modern era of DBS by several decades.[ 5 35 ] Chronic electrical stimulation of the superomedial cerebellar cortex was initially employed over 40 years ago.[ 17 18 ] Overall, cerebellar stimulation has been applied at both the cortical surface[ 20 63 68 120 125 135 ] and deep cerebellar nuclei,[ 108 ] with widely varying degrees of efficacy against seizure activity. Three trials have employed a controlled, double-blind methodology,[ 120 125 135 ] representing a combined experience of 22 patients. Evidence of stimulation efficacy was only found in the study by Velasco and colleagues.[ 125 ] Large-scale blinded clinical trials using current DBS hardware in well-defined patient cohorts remain to be undertaken, mainly due to the ongoing debate about the optimal site of cerebellar stimulation.[ 5 35 ]

Outside the cerebellum, direct stimulation of the hippocampus has also been investigated in epilepsy. Structures of the mesial temporal lobe are a natural target for neuromodulation in view of the proven effectiveness of mesiotemporal resective surgery in patients with temporal lobe epilepsy.[ 5 ] Classically, hippocampal stimulation has been applied to patients with bitemporal seizure foci or at high risk for memory impairment with open surgical resection.[ 5 ] A number of clinical reports have been published on the use of hippocampal DBS so far.[ 14 114 123 124 127 130 ] Notably, in studies by Velasco et al.[ 123 ] and Tellez-Zenteno et al.,[ 114 ] a double-blind stimulation protocol was used, with divergent results: in the former, patients with normal imaging had >95% and patients with hippocampal sclerosis had >50% seizure reduction at long-term follow-up, while in the latter seizure reduction was only 15% with no clear neuropsychological or quality-of-life benefit. Consequently, hippocampal DBS remains investigational, with more data being required to prove efficacy and confirm safety particularly with respect to memory impairment.

Thalamic DBS has increasingly gained importance in the treatment of epilepsy. Following an initial report of success with centromedian (CM) nucleus stimulation,[ 126 ] >50% seizure reduction was demonstrated in two early double-blind trials – one with placebo – employing DBS at the same target.[ 32 57 ] Subsequently, the anterior nucleus (AN) superseded the CM nucleus as the most commonly studied thalamic target for neuromodulation against epilepsy.[ 6 62 ] The Stimulation of the Anterior Nucleus of the Thalamus for Epilepsy (SANTE) trial[ 31 ] enrolled 110 adults with partial or generalized seizures unamenable to conventional resective surgery. Patients underwent bilateral implantation of standard quadripolar DBS electrodes into the AN. During an initial 3-month blinded period, half of the patients received continuous high-frequency stimulation, while the control half were implanted but not stimulated. At 3 months, the stimulated group experienced a significantly greater reduction in seizure frequency compared to unstimulated controls. All patients then went on to receive unblinded stimulation for 2 years. At trial completion, the median overall reduction in seizure frequency was 56%. Additionally, 14 patients were seizure-free and more than half reported seizure reductions of at least 50%.

Other recent novel developments include the responsive neurostimulator, which is an implanted device designed to detect early epileptiform activity and responds – much like a cardiac defibrillator – by delivering pulses of abortive electrical stimulation.[ 112 ] Preliminary studies with such systems are encouraging,[ 107 ] and a randomized, double-blind, multicenter trial evaluating its efficacy is currently underway in the United States.[ 72 ]


With 27 million people currently afflicted worldwide, and a predicted increase in accrual of cases as the world population ages, Alzheimer's Disease (AD) is the most prevalent of neurodegenerative dementias.[ 15 ] A cause of substantial disability and caregiver burden, current medical treatments are largely ineffective at halting its unrelenting course. AD is characterized by pathological changes leading to functional impairment in neural circuits subserving cognitive and memory processes, especially in the hippocampus/entorhinal cortex complex,[ 59 ] as well as cholinergic structures. Turnbull et al.[ 119 ] have used chronic, cyclical, unilateral, monopolar stimulation of the left nucleus basalis of Meynert in a patient with AD. Though they did not find any convincing clinical effect, they observed some evidence of preserved cortical metabolism on serial PET scans.

Based on the serendipitous observation of memory enhancement due to electrical stimulation of the hypothalamic/forniceal region in a patient being treated for obesity,[ 46 ] a phase I trial was conducted using forniceal DBS in six patients with mild-to-moderate Alzheimer′s-type dementia.[ 67 ] Initial results have proved encouraging. Following 1 month of stimulation, PET showed a striking reversal of the typical AD-related glucose hypometabolism in the temporal and parietal cortex. These metabolic changes were sustained at 1 year. Scores on the Mini-Mental Status Exam (MMSE) improved in two patients, and the rate of decline for the group as a whole was slower than expected compared to typical AD patients. No adverse effects attributable to DBS were seen in any patient.


Using neuromodulation to reverse disorders of consciousness caused by traumatic brain injury has been attempted since the 1950s. These early attempts were confounded by the initiation of stimulation in the period soon after brain injury, when some degree of spontaneous recovery is expected, and further weakened by a very limited understanding of the differences in impaired states of consciousness, which may impact recovery and outcome.[ 103 ] The distinction has now been made between a persistent vegetative state (PVS), in which patients demonstrate wakefulness with some degree of sleep–wake cycling but without any environmental awareness, and a minimally conscious state (MCS), in which there is an awareness of the environment despite impaired communication and, importantly, preservation of organized cortical function.[ 39 ] This knowledge, coupled with physiological data implicating the intralaminar nuclei of the thalamus in maintaining wakefulness, arousal, concentration, and attention, paved the way for thalamic DBS as a potential treatment of MCS.[ 121 ] To date, the largest clinical experience with this technique has been from a single center in Japan, with several published reports.[ 118 136 137 ] In the largest and most recent report, the authors describe a total of 26 patients – 21 with PVS and 5 with MCS.[ 137 ] They targeted the mesencephalic reticular formation in two patients and the centromedian–parafascicular (CM–Pf) nuclei of the thalamus in the other 24. Overall, 8/21 PVS recovered the ability to follow verbal commands and 4/5 MCS patients showed sufficient recovery to be discharged from hospital. The experience of this group has been criticized, however, because of the inclusion of several PVS patients and early initiation of DBS within the year following brain injury when spontaneous recovery might still be expected. More recently, considerable interest was generated by a widely publicized case report by Schiff et al.,[ 100 ] who used DBS in intralaminar thalamic nuclei to treat a 38-year-old man exhibiting MCS 6 years after a traumatic brain injury. Using an on–off, double-blind, 6-month crossover design, they reported significant improvement in several objective measures of consciousness with active stimulation. Confirmation of these promising results in larger trials is awaited.


DBS has been shown to be a safe and effective surgical option for a number of movement disorders including essential tremor, PD, and the dystonias. Neural modulation of non-motor circuits is now being investigated for the treatment of several other refractory neurological and psychiatric diseases. Rigorous clinical trials providing robust outcome measures will be needed to establish the safety and efficacy of DBS for these emerging indications.

Publication of this manuscript has been made possible by an educational grant from ELEKTA


1. Aarsland D, Marsh L, Schrag A. Neuropsychiatric symptoms in Parkinson's disease. Mov Disord. 2009. 24: 2175-86

2. Ackermans L, Duits A, Temel Y, Winogrodzka A, Peeters F, Beuls EA. Long-term outcome of thalamic deep brain stimulation in two patients with Tourette syndrome. J Neurol Neurosurg Psychiatry. 2010. 81: 1068-72

3. Ackermans L, Duits A, van der Linden C, Tijssen M, Schruers K, Temel Y. Double-blind clinical trial of thalamic stimulation in patients with Tourette syndrome. Brain. 2011. 134: 832-44

4. Ackermans L, Temel Y, Cath D, van der Linden C, Bruggeman R, Kleijer M. Deep brain stimulation in Tourette's syndrome: Two targets?. Mov Disord. 2006. 21: 709-13

5. Al-Otaibi FA, Hamani C, Lozano AM. Neuromodulation in epilepsy. Neurosurgery. 2011. 69: 957-79

6. Andrade DM, Zumsteg D, Hamani C, Hodaie M, Sarkissian S, Lozano AM. Long-term follow-up of patients with thalamic deep brain stimulation for epilepsy. Neurology. 2006. 66: 1571-3

7. Aouizerate B, Cuny E, Martin-Guehl C, Guehl D, Amieva H, Benazzouz A. Deep brain stimulation of the ventral caudate nucleus in the treatment of obsessive-compulsive disorder and major depression. Case report. J Neurosurg. 2004. 101: 682-6

8. Arnulf I, Ferraye M, Fraix V, Benabid AL, Chabardes S, Goetz L. Sleep induced by stimulation in the human pedunculopontine nucleus area. Ann Neurol. 2010. 67: 546-9

9. Bajwa RJ, de Lotbiniere AJ, King RA, Jabbari B, Quatrano S, Kunze K. Deep brain stimulation in Tourette's syndrome. Mov Disord. 2007. 22: 1346-50

10. Benabid AL, Pollak P, Gervason C, Hoffmann D, Gao DM, Hommel M. Long-term suppression of tremor by chronic stimulation of the ventral intermediate thalamic nucleus. Lancet. 1991. 337: 403-6

11. Benabid AL, Pollak P, Louveau A, Henry S, de Rougemont J. Combined (thalamotomy and stimulation) stereotactic surgery of the VIM thalamic nucleus for bilateral Parkinson disease. Appl Neurophysiol. 1987. 50: 344-6

12. Bewernick BH, Hurlemann R, Matusch A, Kayser S, Grubert C, Hadrysiewicz B. Nucleus accumbens deep brain stimulation decreases ratings of depression and anxiety in treatment-resistant depression. Biol Psychiatry. 2010. 67: 110-6

13. Blahak C, Wohrle JC, Capelle HH, Bazner H, Grips E, Weigel R. Tremor reduction by subthalamic nucleus stimulation and medication in advanced Parkinson's disease. J Neurol. 2007. 254: 169-78

14. Boon P, Vonck K, De Herdt V, Van Dycke A, Goethals M, Goossens L. Deep brain stimulation in patients with refractory temporal lobe epilepsy. Epilepsia. 2007. 48: 551-60

15. Brookmeyer R, Johnson E, Ziegler-Graham K, Arrighi HM. Forecasting the global burden of Alzheimer's disease. Alzheimers Dement. 2007. 3: 186-91

16. Burdick A, Foote KD, Goodman W, Ward HE, Ricciuti N, Murphy T. Lack of benefit of accumbens/capsular deep brain stimulation in a patient with both tics and obsessive-compulsive disorder. Neurocase. 2010. 16: 321-30

17. Cooper IS, Amin I, Gilman S. The effect of chronic cerebellar stimulation upon epilepsy in man. Trans Am Neurol Assoc. 1973. 98: 192-6

18. Cooper IS, Amin I, Riklan M, Waltz JM, Poon TP. Chronic cerebellar stimulation in epilepsy.Clinical and anatomical studies. Arch Neurol. 1976. 33: 559-70

19. Dafotakis M, Fink GR, Allert N, Nowak DA. The impact of subthalamic deep brain stimulation on bradykinesia of proximal and distal upper limb muscles in Parkinson's disease. J Neurol. 2008. 255: 429-37

20. Davis R, Emmonds SE. Cerebellar stimulation for seizure control: 17-year study. Stereotact Funct Neurosurg. 1992. 58: 200-8

21. de Koning PP, Figee M, van den Munckhof P, Schuurman PR, Denys D. Current status of deep brain stimulation for obsessive-compulsive disorder: A clinical review of different targets. Curr Psychiatry Rep. 2011. 13: 274-82

22. Dehning S, Mehrkens JH, Muller N, Botzel K. Therapy-refractory Tourette syndrome: Beneficial outcome with globus pallidus internus deep brain stimulation. Mov Disord. 2008. 23: 1300-2

23. Denys D, Mantione M, Figee M, van den Munckhof P, Koerselman F, Westenberg H. Deep brain stimulation of the nucleus accumbens for treatment-refractory obsessive-compulsive disorder. Arch Gen Psychiatry. 2010. 67: 1061-8

24. Deuschl G, Schade-Brittinger C, Krack P, Volkmann J, Schafer H, Botzel K. A randomized trial of deep-brain stimulation for Parkinson's disease. N Engl J Med. 2006. 355: 896-908

25. Diamond A, Shahed J, Jankovic J. The effects of subthalamic nucleus deep brain stimulation on parkinsonian tremor. J Neurol Sci. 2007. 260: 199-203

26. Diederich NJ, Kalteis K, Stamenkovic M, Pieri V, Alesch F. Efficient internal pallidal stimulation in Gilles de la Tourette syndrome: A case report. Mov Disord. 2005. 20: 1496-9

27. Dougherty DD, Baer L, Cosgrove GR, Cassem EH, Price BH, Nierenberg AA. Prospective long-term follow-up of 44 patients who received cingulotomy for treatment-refractory obsessive-compulsive disorder. Am J Psychiatry. 2002. 159: 269-75

28. Dougherty DD, Weiss AP, Cosgrove GR, Alpert NM, Cassem EH, Nierenberg AA. Cerebral metabolic correlates as potential predictors of response to anterior cingulotomy for treatment of major depression. J Neurosurg. 2003. 99: 1010-7

29. Fava M. Diagnosis and definition of treatment-resistant depression. Biol Psychiatry. 2003. 53: 649-59

30. Ferraye MU, Debu B, Fraix V, Goetz L, Ardouin C, Yelnik J. Effects of pedunculopontine nucleus area stimulation on gait disorders in Parkinson's disease. Brain. 2010. 133: 205-14

31. Fisher R, Salanova V, Witt T, Worth R, Henry T, Gross R. Electrical stimulation of the anterior nucleus of thalamus for treatment of refractory epilepsy. Epilepsia. 2010. 51: 899-908

32. Fisher RS, Uematsu S, Krauss GL, Cysyk BJ, McPherson R, Lesser RP. Placebo-controlled pilot study of centromedian thalamic stimulation in treatment of intractable seizures. Epilepsia. 1992. 33: 841-51

33. Flaherty AW, Williams ZM, Amirnovin R, Kasper E, Rauch SL, Cosgrove GR. Deep brain stimulation of the anterior internal capsule for the treatment of Tourette syndrome: Technical case report. Neurosurgery. 2005. 57: E403-

34. Fontaine D, Mattei V, Borg M, von Langsdorff D, Magnie MN, Chanalet S. Effect of subthalamic nucleus stimulation on obsessive-compulsive disorder in a patient with Parkinson disease. Case report. J Neurosurg. 2004. 100: 1084-6

35. Fountas KN, Kapsalaki E, Hadjigeorgiou G. Cerebellar stimulation in the management of medically intractable epilepsy: A systematic and critical review. Neurosurg Focus. 2010. 29: E8-

36. Freeman RD, Fast DK, Burd L, Kerbeshian J, Robertson MM, Sandor P. An international perspective on Tourette syndrome: Selected findings from 3,500 individuals in 22 countries. Dev Med Child Neurol. 2000. 42: 436-47

37. Garcia-Rill E, Skinner RD. The mesencephalic locomotor region. I. Activation of a medullary projection site. Brain Res. 1987. 411: 1-12

38. Garcia-Rill E, Skinner RD. The mesencephalic locomotor region. II. Projections to reticulospinal neurons. Brain Res. 1987. 411: 13-20

39. Giacino JT, Ashwal S, Childs N, Cranford R, Jennett B, Katz DI. The minimally conscious state: Definition and diagnostic criteria. Neurology. 2002. 58: 349-53

40. Giacobbe P, Mayberg HS, Lozano AM. Treatment resistant depression as a failure of brain homeostatic mechanisms: Implications for deep brain stimulation. Exp Neurol. 2009. 219: 44-52

41. Goldapple K, Segal Z, Garson C, Lau M, Bieling P, Kennedy S. Modulation of cortical-limbic pathways in major depression: Treatment-specific effects of cognitive behavior therapy. Arch Gen Psychiatry. 2004. 61: 34-41

42. Goodman WK, Foote KD, Greenberg BD, Ricciuti N, Bauer R, Ward H. Deep brain stimulation for intractable obsessive compulsive disorder: pilot study using a blinded, staggered-onset design. Biol Psychiatry. 2010. 67: 535-42

43. Greenberg BD, Gabriels LA, Malone DA, Rezai AR, Friehs GM, Okun MS. Deep brain stimulation of the ventral internal capsule/ventral striatum for obsessive-compulsive disorder: worldwide experience. Mol Psychiatry. 2010. 15: 64-79

44. Guridi J, Obeso JA, Rodriguez-Oroz MC, Lozano AA, Manrique M. L-dopa-induced dyskinesia and stereotactic surgery for Parkinson's disease. Neurosurgery. 2008. 62: 311-23

45. Halpern CH, Wolf JA, Bale TL, Stunkard AJ, Danish SF, Grossman M. Deep brain stimulation in the treatment of obesity. J Neurosurg. 2008. 109: 625-34

46. Hamani C, McAndrews MP, Cohn M, Oh M, Zumsteg D, Shapiro CM. Memory enhancement induced by hypothalamic/fornix deep brain stimulation. Ann Neurol. 2008. 63: 119-23

47. Hamani C, Moro E, Lozano AM. The pedunculopontine nucleus as a target for deep brain stimulation. J Neural Transm. 2011. 118: 1461-8

48. Haq IU, Foote KD, Goodman WK, Ricciuti N, Ward H, Sudhyadhom A. A case of mania following deep brain stimulation for obsessive compulsive disorder. Stereotact Funct Neurosurg. 2010. 88: 322-8

49. Hariz MI, Krack P, Alesch F, Augustinsson LE, Bosch A, Ekberg R. Multicentre European study of thalamic stimulation for parkinsonian tremor: A 6 year follow-up. J Neurol Neurosurg Psychiatry. 2008. 79: 694-9

50. Hauser WA. Epidemiology of epilepsy in children. Neurosurg Clin N Am. 1995. 6: 419-29

51. Hauser WA. Recent developments in the epidemiology of epilepsy. Acta Neurol Scand Suppl. 1995. 162: 17-21

52. Hely MA, Reid WG, Adena MA, Halliday GM, Morris JG. The Sydney multicenter study of Parkinson's disease: The inevitability of dementia at 20 years. Mov Disord. 2008. 23: 837-44

53. Holtzheimer PE, Mayberg HS. Deep brain stimulation for treatment-resistant depression. Am J Psychiatry. 2010. 167: 1437-44

54. Houeto JL, Karachi C, Mallet L, Pillon B, Yelnik J, Mesnage V. Tourette's syndrome and deep brain stimulation. J Neurol Neurosurg Psychiatry. 2005. 76: 992-5

55. Huff W, Lenartz D, Schormann M, Lee SH, Kuhn J, Koulousakis A. 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: 137-43

56. Ikemoto S, Panksepp J. The role of nucleus accumbens dopamine in motivated behavior: A unifying interpretation with special reference to reward-seeking. Brain Res Brain Res Rev. 1999. 31: 6-41

57. Jimenez F, Velasco F, Salin-Pascual R, Hernandez JA, Velasco M, Criales JL. A patient with a resistant major depression disorder treated with deep brain stimulation in the inferior thalamic peduncle. Neurosurgery. 2005. 57: 585-93

58. Jimenez-Ponce F, Velasco-Campos F, Castro-Farfan G, Nicolini H, Velasco AL, Salin-Pascual R. Preliminary study in patients with obsessive-compulsive disorder treated with electrical stimulation in the inferior thalamic peduncle. Neurosurgery. 2009. 65: 203-9

59. Kalus P, Braak H, Braak E, Bohl J. The presubicular region in Alzheimer's disease: Topography of amyloid deposits and neurofibrillary changes. Brain Res. 1989. 494: 198-203

60. Karachi C, Grabli D, Bernard FA, Tande D, Wattiez N, Belaid H. Cholinergic mesencephalic neurons are involved in gait and postural disorders in Parkinson disease. J Clin Invest. 2010. 120: 2745-54

61. Kennedy SH, Giacobbe P, Rizvi SJ, Placenza FM, Nishikawa Y, Mayberg HS. Deep Brain Stimulation for Treatment-Resistant Depression: Follow-Up After 3 to 6 Years. Am J Psychiatry. 2011. p.

62. Kerrigan JF, Litt B, Fisher RS, Cranstoun S, French JA, Blum DE. Electrical stimulation of the anterior nucleus of the thalamus for the treatment of intractable epilepsy. Epilepsia. 2004. 45: 346-54

63. Krauss GL, Koubeissi MZ. Cerebellar and thalamic stimulation treatment for epilepsy. Acta Neurochir Suppl. 2007. 97: 347-56

64. Kuhn J, Lenartz D, Huff W, Lee S, Koulousakis A, Klosterkoetter J. Remission of alcohol dependency following deep brain stimulation of the nucleus accumbens: Valuable therapeutic implications?. J Neurol Neurosurg Psychiatry. 2007. 78: 1152-3

65. Kuhn J, Lenartz D, Mai JK, Huff W, Lee SH, Koulousakis A. Deep brain stimulation of the nucleus accumbens and the internal capsule in therapeutically refractory Tourette-syndrome. J Neurol. 2007. 254: 963-5

66. Kurlan R. Clinical practice. Tourette's Syndrome. N Engl J Med. 2010. 363: 2332-8

67. Laxton AW, Tang-Wai DF, McAndrews MP, Zumsteg D, Wennberg R, Keren R. A phase I trial of deep brain stimulation of memory circuits in Alzheimer's disease. Ann Neurol. 2010. 68: 521-34

68. Levy LF, Auchterlonie WC. Chronic cerebellar stimulation in the treatment of epilepsy. Epilepsia. 1979. 20: 235-45

69. Lim AS, Moro E, Lozano AM, Hamani C, Dostrovsky JO, Hutchison WD. Selective enhancement of rapid eye movement sleep by deep brain stimulation of the human pons. Ann Neurol. 2009. 66: 110-4

70. Lopez AD, Murray CC. The global burden of disease, 1990-2020. Nat Med. 1998. 4: 1241-3

71. Lozano AM, Mayberg HS, Giacobbe P, Hamani C, Craddock RC, Kennedy SH. Subcallosal cingulate gyrus deep brain stimulation for treatment-resistant depression. Biol Psychiatry. 2008. 64: 461-7

72. Lyons MK. Deep brain stimulation: Current and future clinical applications. Mayo Clin Proc. 2011. 86: 662-72

73. Maciunas RJ, Maddux BN, Riley DE, Whitney CM, Schoenberg MR, Ogrocki PJ. Prospective randomized double-blind trial of bilateral thalamic deep brain stimulation in adults with Tourette syndrome. J Neurosurg. 2007. 107: 1004-14

74. Mallet L, Polosan M, Jaafari N, Baup N, Welter ML, Fontaine D. Subthalamic nucleus stimulation in severe obsessive-compulsive disorder. N Engl J Med. 2008. 359: 2121-34

75. Malone DA, Dougherty DD, Rezai AR, Carpenter LL, Friehs GM, Eskandar EN. Deep brain stimulation of the ventral capsule/ventral striatum for treatment-resistant depression. Biol Psychiatry. 2009. 65: 267-75

76. Mantione M, van de Brink W, Schuurman PR, Denys D. Smoking cessation and weight loss after chronic deep brain stimulation of the nucleus accumbens: Therapeutic and research implications: Case report. Neurosurgery. 2010. 66: E218-

77. Martinez-Fernandez R, Zrinzo L, Aviles-Olmos I, Hariz M, Martinez-Torres I, Joyce E. Deep brain stimulation for Gilles de la Tourette syndrome: A case series targeting subregions of the globus pallidus internus. Mov Disord. 2011. 26: 1922-30

78. Mayberg HS, Brannan SK, Tekell JL, Silva JA, Mahurin RK, McGinnis S. Regional metabolic effects of fluoxetine in major depression: Serial changes and relationship to clinical response. Biol Psychiatry. 2000. 48: 830-43

79. Mayberg HS, Liotti M, Brannan SK, McGinnis S, Mahurin RK, Jerabek PA. Reciprocal limbic-cortical function and negative mood: Converging PET findings in depression and normal sadness. Am J Psychiatry. 1999. 156: 675-82

80. Mayberg HS, Lozano AM, Voon V, McNeely HE, Seminowicz D, Hamani C. Deep brain stimulation for treatment-resistant depression. Neuron. 2005. 45: 651-60

81. Mazzone P, Sposato S, Insola A, Dilazzaro V, Scarnati E. Stereotactic surgery of nucleus tegmenti pedunculopontine [corrected]. Br J Neurosurg. 2008. 22: S33-40

82. Mian MK, Campos M, Sheth SA, Eskandar EN. Deep brain stimulation for obsessive-compulsive disorder: Past, present, and future. Neurosurg Focus. 2010. 29: E10-

83. Moro E, Hamani C, Poon YY, Al-Khairallah T, Dostrovsky JO, Hutchison WD. Unilateral pedunculopontine stimulation improves falls in Parkinson's disease. Brain. 2010. 133: 215-24

84. Moro E, Lozano AM, Pollak P, Agid Y, Rehncrona S, Volkmann J. Long-term results of a multicenter study on subthalamic and pallidal stimulation in Parkinson's disease. Mov Disord. 2010. 25: 578-86

85. Muller UJ, Sturm V, Voges J, Heinze HJ, Galazky I, Heldmann M. Successful treatment of chronic resistant alcoholism by deep brain stimulation of nucleus accumbens: First experience with three cases. Pharmacopsychiatry. 2009. 42: 288-91

86. Nobler MS, Oquendo MA, Kegeles LS, Malone KM, Campbell CC, Sackeim HA. Decreased regional brain metabolism after ect. Am J Psychiatry. 2001. 158: 305-8

87. Nuttin B, Cosyns P, Demeulemeester H, Gybels J, Meyerson B. Electrical stimulation in anterior limbs of internal capsules in patients with obsessive-compulsive disorder. Lancet. 1999. 354: 1526-

88. Nuttin BJ, Gabriels L, van Kuyck K, Cosyns P. Electrical stimulation of the anterior limbs of the internal capsules in patients with severe obsessive-compulsive disorder: anecdotal reports. Neurosurg Clin N Am. 2003. 14: 267-74

89. Nuttin BJ, Gabriels LA, Cosyns PR, Meyerson BA, Andreewitch S, Sunaert SG. Long-term electrical capsular stimulation in patients with obsessive-compulsive disorder. Neurosurgery. 2008. 62: 966-77

90. Okun MS, Mann G, Foote KD, Shapira NA, Bowers D, Springer U. Deep brain stimulation in the internal capsule and nucleus accumbens region: Responses observed during active and sham programming. J Neurol Neurosurg Psychiatry. 2007. 78: 310-4

91. Last accessed on 2001. Available from: .

92. Orlovsky GN, Severin FV, Shik ML. Locomotion elicited by midbrain stimulation (trans.Russian). Proc Acad Sci USSR. 1966. 169: 1223-6

93. Pahapill PA, Lozano AM. The pedunculopontine nucleus and Parkinson's disease. Brain. 2000. 123: 1767-83

94. Pereira EA, Muthusamy KA, De Pennington N, Joint CA, Aziz TZ. Deep brain stimulation of the pedunculopontine nucleus in Parkinson's disease. Preliminary experience at Oxford. Br J Neurosurg. 2008. 22: S41-4

95. Pisapia JM, Halpern CH, Williams NN, Wadden TA, Baltuch GH, Stein SC. Deep brain stimulation compared with bariatric surgery for the treatment of morbid obesity: A decision analysis study. Neurosurg Focus. 2010. 29: E15-

96. Plaha P, Gill SS. Bilateral deep brain stimulation of the pedunculopontine nucleus for Parkinson's disease. Neuroreport. 2005. 16: 1883-7

97. Porta M, Brambilla A, Cavanna AE, Servello D, Sassi M, Rickards H. Thalamic deep brain stimulation for treatment-refractory Tourette syndrome: Two-year outcome. Neurology. 2009. 73: 1375-80

98. Romigi A, Placidi F, Peppe A, Pierantozzi M, Izzi F, Brusa L. Pedunculopontine nucleus stimulation influences REM sleep in Parkinson's disease. Eur J Neurol. 2008. 15: e64-5

99. Sartorius A, Kiening KL, Kirsch P, von Gall CC, Haberkorn U, Unterberg AW. Remission of major depression under deep brain stimulation of the lateral habenula in a therapy-refractory patient. Biol Psychiatry. 2010. 67: e9-11

100. Schiff ND, Giacino JT, Kalmar K, Victor JD, Baker K, Gerber M. Behavioural improvements with thalamic stimulation after severe traumatic brain injury. Nature. 2007. 448: 600-3

101. Schlaepfer TE, Cohen MX, Frick C, Kosel M, Brodesser D, Axmacher N. Deep brain stimulation to reward circuitry alleviates anhedonia in refractory major depression. Neuropsychopharmacology. 2008. 33: 368-77

102. Schrag A. Quality of life and depression in Parkinson's disease. J Neurol Sci. 2006. 248: 151-7

103. Sen AN, Campbell PG, Yadla S, Jallo J, Sharan AD. Deep brain stimulation in the management of disorders of consciousness: A review of physiology, previous reports, and ethical considerations. Neurosurg Focus. 2010. 29: E14-

104. Servello D, Porta M, Sassi M, Brambilla A, Robertson MM. Deep brain stimulation in 18 patients with severe Gilles de la Tourette syndrome refractory to treatment: The surgery and stimulation. J Neurol Neurosurg Psychiatry. 2008. 79: 136-42

105. Shapiro MB, Vaillancourt DE, Sturman MM, Metman LV, Bakay RA, Corcos DM. Effects of STN DBS on rigidity in Parkinson's disease. IEEE Trans Neural Syst Rehabil Eng. 2007. 15: 173-81

106. Shik ML, Severin FV, Orlovsky GN. Control of walking and running by means of electrical stimulation of the mesencephalon. Electroencephalogr Clin Neurophysiol. 1969. 26: 549-

107. Smith JR, Fountas KN, Murro AM, Park YD, Jenkins PD, Morrell M. Closed-loop stimulation in the control of focal epilepsy of insular origin. Stereotact Funct Neurosurg. 2010. 88: 281-7

108. Sramka M, Fritz G, Galanda M, Nadvornik P. Some observations in treatment stimulation of epilepsy. Acta Neurochir (Wien). 1976. p. 257-62

109. Stefani A, Lozano AM, Peppe A, Stanzione P, Galati S, Tropepi D, Pierantozzi M, Brusa L, Scarnati E, Mazzone P. Bilateral deep brain stimulation of the pedunculopontine and subthalamic nuclei in severe Parkinson's disease. Brain. 2007. 130: 1596-607

110. Stefani A, Pierantozzi M, Ceravolo R, Brusa L, Galati S, Stanzione P. Deep brain stimulation of pedunculopontine tegmental nucleus (PPTg) promotes cognitive and metabolic changes: A target-specific effect or response to a low-frequency pattern of stimulation?. Clin EEG Neurosci. 2010. 41: 82-6

111. Strafella AP, Lozano AM, Ballanger B, Poon YY, Lang AE, Moro E. rCBF changes associated with PPN stimulation in a patient with Parkinson's disease: A PET study. Mov Disord. 2008. 23: 1051-4

112. Sun FT, Morrell MJ, Wharen RE. Responsive cortical stimulation for the treatment of epilepsy. Neurotherapeutics. 2008. 5: 68-74

113. Tabbal SD, Ushe M, Mink JW, Revilla FJ, Wernle AR, Hong M. Unilateral subthalamic nucleus stimulation has a measurable ipsilateral effect on rigidity and bradykinesia in Parkinson disease. Exp Neurol. 2008. 211: 234-42

114. Tellez-Zenteno JF, McLachlan RS, Parrent A, Kubu CS, Wiebe S. Hippocampal electrical stimulation in mesial temporal lobe epilepsy. Neurology. 2006. 66: 1490-4

115. Tierney TS, Sankar T, Lozano AM. Deep brain stimulation emerging indications. Prog Brain Res. 2011. 194: 83-95

116. Timmermann L, Braun M, Groiss S, Wojtecki L, Ostrowski S, Krause H. Differential effects of levodopa and subthalamic nucleus deep brain stimulation on bradykinesia in Parkinson's disease. Mov Disord. 2008. 23: 218-27

117. Torres N, Chabardes S, Benabid AL. Rationale for hypothalamus-deep brain stimulation in food intake disorders and obesity. Adv Tech Stand Neurosurg. 2011. 36: 17-30

118. Tsubokawa T, Yamamoto T, Katayama Y, Hirayama T, Maejima S, Moriya T. Deep-brain stimulation in a persistent vegetative state: Follow-up results and criteria for selection of candidates. Brain Inj. 1990. 4: 315-27

119. Turnbull IM, McGeer PL, Beattie L, Calne D, Pate B. Stimulation of the basal nucleus of Meynert in senile dementia of Alzheimer's type. A preliminary report. Appl Neurophysiol. 1985. 48: 216-21

120. Van Buren JM, Wood JH, Oakley J, Hambrecht F. Preliminary evaluation of cerebellar stimulation by double-blind stimulation and biological criteria in the treatment of epilepsy. J Neurosurg. 1978. 48: 407-16

121. Van der Werf YD, Witter MP, Groenewegen HJ. The intralaminar and midline nuclei of the thalamus.Anatomical and functional evidence for participation in processes of arousal and awareness. Brain Res Brain Res Rev. 2002. 39: 107-40

122. Vandewalle V, van der Linden C, Groenewegen HJ, Caemaert J. Stereotactic treatment of Gilles de la Tourette syndrome by high frequency stimulation of thalamus. Lancet. 1999. 353: 724-

123. Velasco AL, Velasco F, Velasco M, Trejo D, Castro G, Carrillo-Ruiz JD. Electrical stimulation of the hippocampal epileptic foci for seizure control: A double-blind, long-term follow-up study. Epilepsia. 2007. 48: 1895-903

124. Velasco AL, Velasco M, Velasco F, Menes D, Gordon F, Rocha L. Subacute and chronic electrical stimulation of the hippocampus on intractable temporal lobe seizures: preliminary report. Arch Med Res. 2000. 31: 316-28

125. Velasco F, Carrillo-Ruiz JD, Brito F, Velasco M, Velasco AL, Marquez I. Double-blind, randomized controlled pilot study of bilateral cerebellar stimulation for treatment of intractable motor seizures. Epilepsia. 2005. 46: 1071-81

126. Velasco F, Velasco M, Ogarrio C, Fanghanel G. Electrical stimulation of the centromedian thalamic nucleus in the treatment of convulsive seizures: A preliminary report. Epilepsia. 1987. 28: 421-30

127. Velasco M, Velasco F, Velasco AL. Centromedian-thalamic and hippocampal electrical stimulation for the control of intractable epileptic seizures. J Clin Neurophysiol. 2001. 18: 495-513

128. Velasco M, Velasco F, Velasco AL, Boleaga B, Jimenez F, Brito F. Subacute electrical stimulation of the hippocampus blocks intractable temporal lobe seizures and paroxysmal EEG activities. Epilepsia. 2000. 41: 158-69

129. Vonck K, Boon P, Achten E, De Reuck J, Caemaert J. Long-term amygdalohippocampal stimulation for refractory temporal lobe epilepsy. Ann Neurol. 2002. 52: 556-65

130. Vonck K, Boon P, Claeys P, Dedeurwaerdere S, Achten R, Van Roost D. Long-term deep brain stimulation for refractory temporal lobe epilepsy. Epilepsia. 2005. 46: 98-9

131. Weaver FM, Follett K, Stern M, Hur K, Harris C, Marks WJ. Bilateral deep brain stimulation vs best medical therapy for patients with advanced Parkinson disease: A randomized controlled trial. JAMA. 2009. 301: 63-73

132. Welter ML, Mallet L, Houeto JL, Karachi C, Czernecki V, Cornu P. Internal pallidal and thalamic stimulation in patients with Tourette syndrome. Arch Neurol. 2008. 65: 952-7

133. Williams A, Gill S, Varma T, Jenkinson C, Quinn N, Mitchell R. Deep brain stimulation plus best medical therapy versus best medical therapy alone for advanced Parkinson's disease (PD SURG trial): A randomised, open-label trial. Lancet Neurol. 2010. 9: 581-91

134. Wind JJ, Anderson DE. From prefrontal leukotomy to deep brain stimulation: The historical transformation of psychosurgery and the emergence of neuroethics. Neurosurg Focus. 2008. 25: E10-

135. Wright GD, McLellan DL, Brice JG. A double-blind trial of chronic cerebellar stimulation in twelve patients with severe epilepsy. J Neurol Neurosurg Psychiatry. 1984. 47: 769-74

136. Yamamoto T, Katayama Y. Deep brain stimulation therapy for the vegetative state. Neuropsychol Rehabil. 2005. 15: 406-13

137. Yamamoto T, Kobayashi K, Kasai M, Oshima H, Fukaya C, Katayama Y. DBS therapy for the vegetative state and minimally conscious state. Acta Neurochir Suppl. 2005. 93: 101-4

138. Zhou H, Xu J, Jiang J. Deep brain stimulation of nucleus accumbens on heroin-seeking behaviors: A case report. Biol Psychiatry. 2011. 69: e41-2

Leave a Reply

Your email address will not be published. Required fields are marked *