Deep brain stimulation: Current status - CyberLeninka

9Neurology India / January 2015 / Volume 63 / Issue 1

Address for correspondence: Dr. Sanjay Pandey, Department of Neurology, Govind Ballabh Pant Postgraduate Institute of Medical Education and Research, New Delhi ‑ 110 001, India. E‑mail: [email protected].

ABSTRACTIn the last two decades, applications of deep brain stimulation (DBS) have expanded rapidly in the field of neurosciences. The most common indications for DBS are Parkinson’s disease, medically refractory seizures, essential tremors, and primary dystonia. This device has also been used as an investigational tool in patients having Tourette’s syndrome, tardive dyskinesia, and refractory seizures. In the field of psychiatry, DBS has been used for the treatment of refractory obsessive compulsive disorder and depression. The complications are mainly related to surgery, the device, and its stimulation. This article provides an overview of the current status and recent advances in the field of DBS.

Key words: Parkinson’s disease; dystonia; tremor; device; surgery

Introduction

Deep brain stimulation (DBS) is a safe and effective treatment modality for certain neurological and psychiatric disorders. In the 1960s, ablative stereotactic surgery was employed for a variety of movement disorders including Parkinson’s disease (PD), but was largely abandoned in the 1970s because of introduction of highly effective drugs like levodopa. In due course, however, it became obvious that levodopa and other anti‑Parkinsonian drugs produced complications such as motor fluctuations, dyskinesias, hallucination, and psychosis, thereby limiting their utility. This led to a resurgence of surgical modalities as treatment options. Surgeons initially utilized ablative procedures; more recently, DBS has largely replaced the ablative methods as the procedure of choice as it is much less invasive. It is also reversible and adjustable.

The turning point for the utilisation of DBS in the management of movement disorders was the publication by Benabid et al. in 1987 on the efficacious stimulation of ventral intermediate

nucleus of the thalamus for treatment of PD.[1] Subsequently, Bergman et al. in 1990 and Aziz et al. in 1992 demonstrated the efficacy of selective bilateral subthalamic nuclear (STN) lesioning in the treatment of primates in whom Parkinsonism had been artificially developed with the help of the neurotoxin, 1‑methyl‑4‑phenyl‑1,2,3,6‑tetrahydropyridine (MPTP).[2,3]

Since its approval by the Food and Drug Administration (FDA) for PD in 2002, DBS has become a viable therapeutic modality for patients suffering from neurological and psychiatric disorders.

Technique

In the DBS procedure, the stimulation electrodes are implanted into specific regions of the brain. An implanted, externally programmable pulse generator delivers continuous high‑frequency electrical stimulation akin to a cardiac pacemaker.[4] The aim of DBS is to alter the physiology of a group of neurons within the basal ganglia or the thalamus. The localization is done by radiological and physiological landmarks. The radiological localization is performed by identifying the anterior commissure (AC), posterior commissure (PC), and the border between the internal capsule (IC) and the thalamus by using both computed tomography (CT) and magnetic resonance imaging (MRI) scans through a CT/MRI fusion technique. Stereotactic ventriculography provides a better localization, but is not the

Deep brain stimulation: Current statusSanjay Pandey, Neelav Sarma

Department of Neurology, Govind Ballabh Pant Postgraduate Institute of Medical Education and Research, New Delhi, India

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Pandey and Sarma: Deep brain stimulation

Neurology India / January 2015 / Volume 63 / Issue 1

currently preferred technique because it is invasive and may not always be successful due to the difficulty encountered in cannulating an undilated ventricle.[5] Physiological localization helps in identifying different basal ganglia and thalamic nuclei on the basis of their electrophysiological properties. These properties include spontaneous activity, neuronal response to passive and active movements, and sensory responses to natural or electrical stimulation. Microelectrodes are used to isolate single action potentials.[6‑8] These microelectrodes have a high impedance, facilitating isolation of single frequencies.[9] The STN is localized by its typical firing patterns (bursting pattern characterized by asymmetrical spikes at high frequency which shows proprioceptive response to passive movements). Since substantia nigra pars reticularis is immediately below the STN, it is important to recognize the neuronal activity of substantia nigra also (symmetrical spikes having a large amplitude with no response to external stimuli).[5] The electrode implantation is preferably performed under local anesthesia. Occasionally, this may also be done under general anesthesia, but the beneficial effects of DBS on the patient’s symptoms will not be apparent during surgery. After establishing multiple tracks using physiological localization, the neurophysician directly assesses the effects of DBS at various locations. This is the most important step in deciding the site of microelectrode placement and is pivotal for the success of the DBS procedure. Testing for rigidity of movements at the wrist is the easiest way to assess the beneficial effects of surgery as it does not require the active participation of the patient. Tremor may also be assessed during surgery; however, intraoperative assesment of speech and bradykinesia is difficult. Once the best track with maximal beneficial and minimal side effects has been established, the microelectrode is replaced by a lead that is fixed to the skull. Following the successful intracranial lead placement, a pulse generator is placed at the subclavian region in a subcutaneous pouch under general anesthesia. However, some groups prefer to perform this step a week after the insertion of the electrode. A postoperative MRI helps in ensuring proper placement of the electrodes within the brain. The next important step is the programming of the device in which the neurophysician adjusts the voltage, frequency, and polarity settings to achieve the best possible outcome [See Table 1].

Mechanism of Action

The exact mechanism by which DBS exerts its action is still not clear. It has been proposed that its effects depends on stimulation rather than creation of a lesion. Mechanisms by which it produces a functional inhibition include 1) neuronal message jamming (that is transmitted through the stimulated

structure) and desynchronization of abnormal oscillations;[10‑12] (2) inhibition of neuronal firing;[13,14] (3) combined induction and excitation of high‑frequency bursts; and, (4) inhibition of neurotransmitter release.[15]

DBS in PDThe preferred targets for DBS in PD patients are the bilateral subthalamic nuclei. The response to DBS is quantified by a unified PD rating scale (UPDRS). It is divided into part I, II, III, and IV that assess non‑motor experiences, motor experiences, motor examination, and drug‑induced dyskinesias (including motor fluctuations), respectively. Patients with PD who have cardinal symptoms of the disease are likely to improve significantly.[16‑18] Patients showing significant improvement with the optimum adjustment of anti‑PD drugs are likely to show a similar improvement after proper placement of the electrodes within the STN.[19,20] Studies have shown unequivocal improvement in patients in part II and III UPDRS.[21‑24] DBS alleviates the same symptoms of PD that are relieved by levodopa. In addition, DBS also helps in reducing dyskinesias and non‑dopa‑responsive tremors. The contraindications to its usage include the presence of dementia and cognitive deficits. These features may get exacerbated after a DBS procedure. Stimulation of either the STN or the globus pallidus internus (Gpi) has shown statistically significant improvement in the UPDRS scores.[25] Comparison between the effects of the two stimulation sites have not shown any superiority of one over the other.[26] In a study, 159 patients were randomly assigned to Gpi (n = 89) and STN (N = 70) DBS. At a follow‑up after 36 months, the motor symptoms were

Table 1: Post procedural programming of the deep brain stimulation (DBS) hardware[97]

PatientUsually 3–4 weeks after the surgery (so that any micro‑lesional effects may be over by that time)Initial stimulation is done in the ‘off’ state

Electrode configurationUse pseudo‑monopolar configuration to assess effect and side‑effect threshold, and gradually increase the amplitudeDecide whether bipolar versus monopolar configuration is more useful using microelectrode recording data obtained during surgeryFrequency, pulse duration, and voltage setting depend on the indications and may be different for each individual patient

EffectEasiest effect to monitor is tremorRigidity is a close secondBradykinesia is unreliableEffect on dystonia may take weeks to months

Associated problems during the initial stimulationDyskinesia may worsen transiently, which is considered as a good prognostic markerRapid tapering of dopaminergic drugs may be considered in such patients

DBS ‑ Deep brain stimulation


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stable and did not differ in the two groups.[27] However, one study has found that STN stimulation achieves a greater improvement in the UPDRS and the other disability scores and also ensures a more sustained benefit through medicines for PD.[28] A high baseline score on section III (motor) of the UPDRS and good baseline levodopa responsiveness are independent predictors of a greater improvement in the motor score after surgery.[5] The other candidates in whom DBS shows a sustained benefit include those with motor fluctuations and dyskinesias who do not respond well to medical therapy.[29,30] In a recent study, neurostimulation was studied in patients with PD with early motor fluctuation. STN stimulation was found to be superior to the medical therapy in them.

Several studies and a meta‑analysis have indicated that there was a significant improvement in the UPDRS part II and part III scores and also reduction in the medication administered in the “off period” following the DBS when compared to the pre‑surgery medication being administered for the same state.[16,17,31] The reduction (43–57%) in part III UPDRS was also found to be sustained in studies where patients were followed up for 2–4 years.[32‑38] Tremor and rigidity were found to have an improvement of 70–75%, while akinesia improved by 50% in a study.[16] The mean reduction in the postoperative levodopa requirement was in the range of 50–56%.[17,31] There was a reduction of levodopa‑induced dyskinesias and in their duration by 69% and 71%, respectively.[17,37] One

Table 2: Recent studies of deep brain stimulation in Parkinson’s disease

Study Study type Target Number Follow‑up (years)

Results Complications

Tir 2007 Prospective study STN 100 PD 1 in UPDRS (III) 43%,(II) 34% and dyskinesia‑related disability by 61%

Infection (7), intracerebral hematoma (5), electrode failure (4), incorrect lead placement (8)

Romito 2009 Prospective study STN 20 PD 5 UPDRS 54.2%LED by 61.9%

Data not available

Weaver 2009 Multi‑center RCT STN=60Gpi=61

255 APD DBS group gained 4.6 h/d without troubling dyskinesia and non DBS 0 h/d

39 AEs and 1 death

Okun 2009 Prospective blinded study for mood and cognition

Unilateral GPi (23), STN (22)

45 PD 7 months in UPDRS motor score same in two groups

No effect on mood, cognition on optimal stimulation.Ventral stimulation caused less energy, less happy disposition.Verbal fluency worse in 3 STN DBS

Moro 2010 Multi‑center prospective

Bilateral STN (35)Gpi‑16

51 PD 5‑6 in UPDRS (III). In both groups, dyskinesias and ADL improved.Anti‑PDmedications in STN group only

Adverse events were more frequent in the STN group

William 2010 PD‑SURG trial at 13 centres randomized, open‑label

STN surgery and Medical (183) vs. Medical alone (183)

366 PD 1 Mean improvement in PDQ‑summary index score more in surgical group

36 (19%) patients had serious surgery‑related AEs

Follett 2010 13 centers RCT STN‑147GPi‑152

299 PD 2 No difference in UPDRS (III) in STN, GPi groups (P=0.50). STN patients required less dopaminergic drugs

Visuomotor processing speed decline (P=0.03), depression (P=0.02) more in STN group. Serious AEs more in STN (56%) than GPi (51%)

Kishore 2010 Single blind and open‑label

All bilateral STN 45 PD 5 Benefits of simulation substantial on motor complications and QOL

procedure‑related AEs (9), device related AE (5) and stimulation related AE (57)

Okun 2012 Prospective multi‑centric RCT

STN CC 136 STNCC

1 UPDRS (III) improved by 39% Infection (5), ICH (4)

Weaver et al. 2012

Multi‑center RCT Bilateral STN (70) GPi (89)

159 PD 3 UPDRS (III) improvement from baseline almost similar in STN and GPi

Mattis dementia rating scale declined faster for STN than GPi (P=0.01)

Odekerken 2012

NSTAPS study : RCT STN‑63GPi‑65

128 APD 1 STN>GPi in UPDRS (III) mean change, ALDS score, medication reduction

No differences in AEs

Schuepbach 2013

EARLYSTIMRCT

Bilateral STN 251 PD 2 in PDQ (39%), UPDRS‑II, III and medication

AE similar in neurostimulation and medication group

DBS ‑ Deep brain stimulation, STN ‑ Subthlamic nucleus, Vim ‑ Ventral intermediate nucleus, PD ‑ Parkinson’s disease patients, APD ‑ Advanced PD patients, ‑ Decrease, UPDRS ‑ Unified Parkinson’s disease rating scale, LED ‑ Levodopa equivalent dose, AE ‑ Adverse events, GPi ‑ Globus pallidus internus, QOL ‑ Quality of life, ALDS ‑ Academic Medical Center Linear Disability Scale, PDQ ‑ Parkinson’s Disease Questionnaire, ICH ‑ Intracerebral hemorrhage, STNCC ‑ STN constant current


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Table 3: DBS in Parkinson’s disease: Recommendations (EFNS) 2014[98]

The procedure is only recommended for patients (<70 years) without major psychiatric or cognitive problems who have

Severe motor fluctuationsSTN or Gpi DBS is effective against motor fluctuations and dyskinesia (Level A)

Unpredictable on‑offSTN DBS is effective (Level A)

DyskinesiasSTN DBS allows reduction in the dopaminergic treatment (Level A)Gpi stimulation may reduce severe dyskinesias (Level A)

Biphasic dyskinesiaSTN DBS is effective (Level A)

Off‑period and early morning dystoniasSTN or Gpi DBS is effective (Level A)

STN ‑ Subthalamic nuclear, DBS ‑ Deep brain stimulation, GPi ‑ Globus pallidus internus, EFNS ‑ European Federation of Neurological Societies

of the symptoms that improves less when compared to the other ones is speech.[16] As a result of involvement of the cortico‑bulbar fibres the patients may have increased dysarthria.[38] In terms of quality of life, a multicentric trial compared the impact of DBS along with optimal medical therapy versus optimal medical therapy alone and found greater improvement in mobility, activities of daily living, emotional well‑being, stigma, and bodily discomfort in the former group when compared to the medical therapy alone.[17] Factors that predict response to DBS include the age of the patient and his/her response to levodopa therapy.[19,39] An age of less than 65 years predicts an improvement in the quality of life; good results, however, have also been reported in patients in a more advanced age.[23] Factors such as freezing of gait that do not respond to levodopa also respond poorly to DBS therapy [Tables 2 and 3].[40]

DBS in dystoniaBefore DBS, apart from botulinum toxin, there were hardly any options available for patients with dystonia (especially generalized dystonias). The preferred site for DBS in dystonic patients is the GPi in the basal ganglia; however, STN stimulation has also been successfully used.[40‑43] DBS produces a good response in patients having a primary dystonia, especially generalized dystonia. The other types of dystonia where it is also effective include the cervical dystonias and tardive dystonia.[44‑46] Results are better in young patients with a shorter disease duration.[47] Moreover, unlike other diseases, the beneficial effect of DBS in dystonia is delayed by weeks or months after the procedure.[48] The target localization of GPi for DBS in dystonic patients is difficult to achieve as compared to the STN localization in patients with PD. This is because younger patients manifesting a dystonia have difficulty in cooperating during the awake surgery; no definite thumbprint of the neurophysiological target is available; and, no intraoperative changes occur on stimulating the target site. Nevertheless, studies have demonstrated a 50% reduction in the disability of patients suffering from primary generalized dystonia.[49] Similarly, patients having a cervical or tardive dystonia improve by 40–90%.[50] The Burke–Fahn–Marsden Dystonia Rating Scale (BFMDRS) for evaluating generalized dystonia, and the Toronto Western Spasmodic Torticollis Rating Scale (TWSTRS) for assessing cervical dystonia, are useful tools to grade the severity of the disease and the response to treatment.[51‑54] DBS has also been found to have long‑term beneficial effects.[55‑58] Results in secondary dystonia have also been encouraging. In a study of 13 consecutive patients (that included 9 patients having a secondary dystonia), 11 had global subjective gains and notable objective improvement, but the benefits were variable and not completely predictable.[59] In another study, bilateral Gpi DBS was performed in adults

with dystonic‑choreoathetotic cerebral palsy. There was a significant improvement in pain, functional disability, and mental health‑related quality of life.[60] In a multicentric (16 centers) study, 23 patients having neurodegeneration due to iron accumulation in the brain were treated with bilateral GPi DBS. At a follow up of 9–15 months, 66.7% of patients had 20% or more improvement in the severity of dystonia and 31.3% had 20% or more improvement from their pretreatment disability status.[61] In another multicentric study of 15 patients of choreoacanthocytosis who underwent DBS of the GPi, the short‑ and long‑term outcomes were analyzed. These patients had a significant improvement in their unified Huntington’s disease motor and functional capacity scores [Tables 4 and 5].[62]

DBS in tremorBesides the resting tremors in PD, other tremor types amenable to DBS include the essential tremors (ET), cerebellar tremors, and Holmes’ tremors. In spite of the multiple pharmacological options available for ET, the symptoms in the vast majority of the patients are not well controlled. The targets for DBS in this condition are the ventral intermediate (Vim) nucleus of the thalamus and the STN. Vim-DBS has been found to be effective in ET.[63,64] It has a beneficial effect on appendicular, head, and vocal tremors.[65] Studies have shown unequivocal improvement in tremors that are otherwise refractory to medical therapy.[66‑68] In a study, Vim‑DBS reduced the amplitude, frequency, regularity, and tremor‑EMG coherence of ET in comparison to controls.[69] Pharmacological treatment fails to change the characteristics of tremor other than in reducing its amplitude. Studies have also shown a better response in bilateral thalamic stimulation as compared to unilateral thalamic stimulation.[70] The tremor control has been found to be sustained for up to 6 years following


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such as Holmes tremor have also been found to respond well to DBS.[73] Recent studies have shown a trend toward better response to zona incerta stimulation when compared to STN stimulation [Tables 6 and 7].[74,75]

DBS in Psychiatric Disorders

DBS has also been found to be useful in certain psychiatric conditions such as obsessive compulsive disorders (OCD), Tourette’s syndrome, and depression. The target for DBS in OCD is the anterior limb of IC.[1] DBS provides a sustained relief over a long period of time.[76] DBS has been found to be a viable option in patients suffering from Tourette’s syndrome who have persistent symptoms in spite of optimized medical therapy. The plausible targets for DBS in this condition include the midline intralaminar nuclei of the thalamus, the motor and limbic portions of GPi, and the anterior limb of the IC.[77,78] Significant improvement in motor

Table 4: Recent studies of deep brain stimulation in dystonia

Study Type of study Target of stimulation Number of patients Followup ResultsMueller 2008 Randomized active‑sham

stimulation trialGPi chronic high‑frequency stimulation

40 patients of medically refractory primary generalized (24) or segmental dystonia (16)

6 months Significant reduction in BFMDRS movement score, SF‑36

Magariños‑Ascone 2008

Prospective study GPi 10 2 years BFMDRS movement score improved significantly

Pretto 2008 Prospective blinded study

GPi 13 (secondary dystonia‑9, spasmodic torticollis‑ 4)

5.9 months Marked (7), moderate (3), slight (1) improvement

Moro 2009 Prospective study GPi 8 (Cervical dystonia) TWSTRS severity scores decreased by 56.7%

Sensi 2009 Prospective study GPi 11 (Segmental dystonia) 36 months Significant improvement in BFMDRS score

Gruber 2009 Prospective study GPi 9 (Tardive dystonia) 18‑80 months

BFMDRS motor score decreased by 56.4% and disability score by 62.5%

Vidailhet 2009 Multicentre prospective pilot study

GPi 13 (Dystonia‑choreoathetosis in cerebral palsy)

1 year Mean BFMDRS score improved, but was not significant (P=0.009)

Timmerman 2010 Multicentre prospective pilot study

GPi Neurodegeneration with brain iron accumulation: 23

9‑15 months

Mean BFMDRS score improved but was not significant

Reese 2011 Multicentre prospective case series

GPi Meige syndrome: 12 78 months Mean BFMDRS score improved 45% at short term and 53% at long term follow‑up

Ostrem 2011 Prospective pilot study STN Cervical dystonia: 9 1 year TWSTRS total score improved significantly

Skogseid 2012 Prospective blinded study GPi Cervical dystonia: 7 12‑48 months TWSTRS total score improved by 70%Markun 2012 Prospective study GPi DYT1: 14 6 years BFMDRS score improvedVolkman 2012 Multicenter randomized

controlled trialGPi 40 recruited and 38 agreed to

follow‑up5 years BFMDRS score improved significantly

Schjerling 2013 Prospective double‑blind crossover study

STN and GPi with alternate stimulation

12 patients with focal, multifocal, or generalized dystonia

6 months each

BFMDRS movement scores, quality of life physical scores improvedAcceptance rate better for STN

Miquel 2013 Multicenter prospective study

GPi Chorea acanthocytosis: 15 29.5 months

Unified Huntington’s Disease RatingScale‑Motor Score reduced

Ostrem 2014 Blinded prospective study

Low frequency then high frequency STN

Primary generalized dystonia: 7 3, 6, &12 months

BFMDRS and TWSTRS improved significantly

Volkman 2014 randomized, sham‑controlled trial

32 stimulation, 30 sham stimulation

62 patients 3 months Pallidal stimulation better than sham stimulation

DBS ‑ Deep brain stimulation, STN ‑ Subthlamic nucleus, Vim ‑ Ventral intermediate nucleus, BFMDRS ‑ Burke–Fahn–Marsden Dystonia rating scale, TWSTRS ‑ Toronto western spasmodic torticollis rating scale, DYT1 ‑ Early onset primary dystonia

the implantation.[71] In a study, 25 out of 39 patients (20 PD, 19 ET) with electrode implantations in the Vim were evaluated at 2 and 6–7 years.[72] Kinetic and postural tremors improved (P < 0.025) at follow up in patients suffering from ETs and there was also a significant improvement in functions of their hands (P < 0.025). Other types of tremors

Table 5: Deep brain stimulation in dystonia: Recommendations (EFNS)2011[99]

Globus pallidus interna DBS is a good treatment option for primary generalized or segmental dystonia, once medication including botulinum toxin has failed (Level A)Gpi DBS is a good treatment option for cervical dystonia once medication including botulinum toxin has failed (Level B)In secondary dystonia other than tardive dystonia, Gpi DBS is less effective (Level C)The procedure is not without side effects and requires a multidisciplinary team with specialized expertise (good clinical practice)GPi ‑ Globus pallidus internus, DBS ‑ Deep brain stimulation, EFNS ‑ European Federation of Neurological Societies


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and vocal tics has been found following the DBS with the reduction of sensory urge that accompanies such patients. The DBS target for depression, unlike the psychiatric conditions mentioned above, is not well defined. A study of six patients with refractory depression found some clinical benefit in stimulating the subgenual cingulate region.[79]

Complications of DBS

Surgery-related complicationsHemorrhageThe occurrence of intracerebral hemorrhage has been found in up to 4.5% patients in various studies.[80‑83] Symptomatic hemorrhage has been found to be present in 2% of the cases, while 1.3% have an asymptomatic hemorrhage.[81] The important risk factors for hemorrhage in this setting include hypertension and an elderly age. The technical risk factors include a misplaced sulcal or ventricular trajectory [Table 8].[84]

InfectionA meta‑analysis of 35 open label trials found the incidence of infection in 4.7% of the patients following the DBS procedure.[26,85] No significant difference in the infection rate was found in

patients receiving the STN stimulation versus those receiving the GPi stimulation.[86] The highest risk of infection was in the first month following surgery.[85] The intracranial components of DBS are less likely to get infected when compared to the connector and the subcutaneous pocket lodging the implanted programmable generator.[87] Studies have reported a reduction in infection rates by local application of neomycin–polymyxin.[88]

DeathThe rate of death ranges from 0 to 4.4%.[89,83] This variability may be explained by the different inclusion criteria used in assessing perioperative complications such as myocardial infarction, pulmonary embolism, and pneumonia.[89‑91]

Other surgery- and hardware-related complicationsRare complications of surgery include cerebrospinal fluid leak, pneumonia, and pulmonary embolism. Hardware‑related complications are rare and include lead fracture and migration, erosion, and malfunction of the device.

Electrical stimulus related complicationsDepressionA meta‑analysis of 1398 patients found the incidence of depression to be approximately 8% in patients after the DBS procedure.[26,92] It could not be established whether this symptom was due to the procedure of DBS or it was a part of the progressive neuronal loss that occurs in conditions like PD.[26,93]A comparative analysis between the STN and GPi DBS found an increased incidence of depression in the former group 24 months following the procedure. The incidence of suicides has been found to be higher in patients who receive STN DBS when compared to the general population and patients treated for PD.[26]

Table 6: Important studies of deep brain stimulation in essential tremor

Study Type of study Target of stimulation Number of patients Follow‑up ResultsHubble 1996 non‑blinded

interventionalVim nucleus of thalamus 10 medically refractory

patients of ET1, 3, and 6 months An effective and safe modality for

treatment of essential tremorKoller 1999 Partially blinded,

interventionalVim nucleus of thalamus 38 patients with essential

head tremorAt 3,6,12 months DBS to be considered in head

tremor refractory to medicationOndo 2001 Open and blinded,

case controlUnilateral vs bilateral thalamic stimulation

13 patients with essential tremor

At 0, and 3 months Bilateral thalamic DBS better than unilateral DBS in controlling appendicular, midline ET tremors

Koller 2001 Observational study Vim nucleus of the thalamus

25 patients of DBS 2 years after implantation

Tremor scores were significantly improved at long‑term follow‑up

Rehncrona 2003 Double‑blind assessment

VIM thalamic nucleus 19 patients with essential tremor

2 years and 6–7 years Significant improvement in kinetic and positional tremor

Vaillancourt 2003 Randomized control trial

VIM thalamic nucleus 6 patients on DBS and off DBS with matched controls

DBS improved the tremor

Lee 2005 Interventional prospective study

thalamus 19 patients of DBS 10–75 months Thalamic DBS effective and safe

Blomstedt 2010 Prospective study posterior subthalamic area

21 patients with essential tremor

1 year 60% improvement in essential tremor rating scale

Blomstedt 2011 Prospective study STN vs the zona incerta 4 patients Czi DBS more efficient than STN

DBS ‑ Deep brain stimulation, STN ‑ Subthalamic nucleus, Vim ‑ Ventral intermediate nucleus, ET ‑ Essential tremor, Czi ‑ Zona incerta

Table 7: Deep brain stimulation in essential tremor: Recommendations (American Academy of Neurology 2011)[100]

DBS of ventrointermediate nucleus of thalamus effectively treats contralateral limb tremors in ET that is refractory to medical management (Level C)Relative advantages and disadvantages of unilateral vs bilateral DBS in the treatment of limb tremor exist (Level U)Direct subthalamic stimulation and/or zona incerta/prelemniscal stimulation is recommended (Level U)DBS ‑ Deep brain stimulation, ET ‑ Essential tremor, VIM ‑ Ventrointermediate nucleus


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Language and speechDBS, especially of the STN, has been associated with decreased verbal fluency. It is, however, unclear whether this complication is due to the procedure itself or occurs as a result of decreasing the dopaminergic medications following the DBS procedure.[26,94]

A study on the effects of DBS on STN found speech intelligibility to be reduced by an average of 14.2% ± 20.15% without medication, and by 16.9% ± 21.8% when continued on medication 1 year after the DBS. A decrease of 3.6% ± 5.5% and 4.5% ± 8.8%, respectively, was observed in the non‑surgical control group during the same period.[95] Medially located

electrodes were associated with a higher risk of speech deterioration.

Gait abnormalitiesDBS especially of the STN has been found to be associated with an increased incidence of postural instability and gait dysfunction.[26] Similar to language dysfunction, it is unclear whether these deficits appear as a result of the stimulation itself or as a result of decrease in the usage of dopaminergic medications. Patients who undergo DBS of the GPi, however, appear relatively resistant to these abnormalities.[81,96]

Conclusion

DBS is evolving as an effective treatment modality in certain neurological and psychiatric conditions. It has become an indispensible option for patients who are otherwise refractory or have a poor response to medical therapy. With proper preoperative selection and follow‑up, it can be the key to a better lifestyle for patients whose disability may not improve with medications [Table 9 and 10].

References

1. 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;50:1-6, 344-6.

2. Bergman H, Wichmann T, DeLong MR, Reversal of experimental Parkinsonism by lesions of the subthalamic nucleus. Science 1990;249:4975, 1436-8

3. Aziz TZ, Peggs D, Agarwal E, Sambrook MA, Crossman

Table 8: Important studies of deep brain stimulation related complications

Study Type of study Number of patients and follow‑up

Results

Bloomstedt 2005 Prospective clinical study 119 patients, 10 years 15% had hardware‑related complications, majority occurred within the first 4 years

Hamani 2006 Review study 922 patients with DBS Infections in 6.1%, migration or misplacement of the leads in 5.1%, lead fractures in 5.0% , erosion in 1.3%

Temel 2006 Retrospective study 1398 patients of STN DBS Cognitive problems in 41%, depression in 8%, mania in 4%, anxiety <2%York 2008 Prospective case control study 51 PD patients, 6 months Significant decline in verbal fluency, inhibition of dominant responseWeaver 2009 Randomized controlled trial 255 PD , 3 and 6 months Surgical site infection (9%), surgical site pain (9%), nervous system (15),

psychiatric (11), device related (8), cardiac (4) complicationsGeravis 2009 Long‑tem prospective study 42 advanced PD patients ICH (2), device infection (3), phlebitis (2), pulmonary embolism (1),

dysarthria (56%), depression (39%), eyelid opening apraxia (30.4%), apathy (4.3%)

Boviastis 2010 Retrospective study 106 PD patients Procedure‑related complications in 11.3% of patients, hardware complications in 4.3% of the procedures

St George 2010 Meta‑regression long term study

Included 11 articles PIGD was worse than presurgery function within 2 years. GPi patients showed no significant long‑term decline in PIGD

Follett 2010 Multicenter, randomized, blinded

255 PD patients, upto 24 months

Serious adverse event in up to 50% of cases, no significant difference between pallidal and subthalamic stimulation

Tripoliti 2011 Case control clinical study 15 PD patients, 1 year Speech deterioration and high risk of poor speech outcomeZrinzo 2012 Meta‑analysis 214 PD patients Hemorrhage in 5%, symptomatic in 2.1%, permanent deficit in 1.1%DBS ‑ Deep brain stimulation, STN ‑ Subthalamic nucleus, GPi ‑ Globus pallidus internus, PIGD ‑ Postural instability and gait disability, ICH ‑ Intracerebral hemorrhage

Table 9: Search strategy and selection criteria

PubMed was searched from 1st January 1989 to 10th November 2014. A total of 8248 articles on ‘deep brain stimulation’, 1945 articles on ‘deep brain stimulation in neurology’ and 728 articles on ‘deep brain stimulation in psychiatry’ were found. The articles included in the study were based on the discretion of the authors.

Table 10: Evidence classification[98‑100]

Class I: Prospective, randomized, controlled clinical trial, which is adequately powered has defined outcome and inclusion/exclusion criteriaClass II: Prospective matched group cohort studyClass III: All other controlled trialsClass IV: Evidence from uncontrolled trials, case reports/series or expert opinionLevel A rating (established as effective) requires at least one convincing class I studyLevel B rating (probably effective) requires at least one convincing class II study or overwhelming class III evidenceLevel C rating (possibly effective) requires at least two convincing class III studiesLevel U rating (insufficient evidence to support or refute)


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How to cite this article: Pandey S, Sarma N. Deep brain stimulation: Current status. Neurol India 2015;63:9-18.

Source of Support: Nil, Conflict of Interest: None declared.


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Deep brain stimulation: Current status - CyberLeninka

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