Archived Policies - Surgery
Deep Brain Stimulation for Tremor
This medical document is no longer scheduled for routine literature review and update.
Unilateral deep brain stimulation (DBS) of the thalamus may be considered medically necessary in patients with disabling, medically unresponsive tremor due to essential tremor or Parkinson’s disease (PD).
Unilateral or bilateral DBS of the globus pallidus or subthalamic nuclei may be considered medically necessary in patients with PD with all of the following:
Unilateral or bilateral DBS of the globus pallidus or subthalamic nuclei may be considered medically necessary in patients aged seven years or greater with chronic, intractable (drug refractory) primary dystonia, including generalized and/or segmental dystonia, hemidystonia or cervical dystonia (torticollis).
Deep brain stimulation for other movement disorders, including but not limited to multiple sclerosis (MS) and post-traumatic dyskinesia, is considered experimental, investigational and unproven.
Deep brain stimulation for the treatment of chronic cluster headaches is considered experimental, investigational and unproven.
NOTE: Replacement, revision or removal of electrodes and/or pulse generator for deep brain stimulation will not require additional medical necessity review.
Deep brain stimulation has been investigated as an alternative to permanent neuroablative procedures, such as thalamotomy and pallidotomy. The technique has been most thoroughly investigated as an alternative to thalamotomy for unilateral control of essential tremor and tremor associated with PD. More recently, there has been research interest in the use of DBS of the globus pallidus or subthalamic nucleus as a treatment of other parkinsonian symptoms, such as rigidity, bradykinesia, or akinesia. Another common morbidity associated with PD is the occurrence of motor fluctuations, referred to as "on and off" phenomena, related to the maximum effectiveness of drugs (i.e., the ‘on’ state) and the nadir response during drug troughs (i.e., the ‘off ‘state). In addition, levodopa, the most commonly used anti-Parkinson's drug, may be associated with disabling drug-induced dyskinesias. Therefore, the optimal pharmacologic treatment of PD may involve a balance between optimal effects on Parkinson's symptoms versus the appearance of drug-induced dyskinesias. The effect of DBS on both Parkinson's symptoms and drug-induced dyskinesias has also been studied.
DBS has also been investigated in patients with primary dystonia, defined as a neurological movement disorder characterized by involuntary muscle contractions, which force certain parts of the body into abnormal, contorted, and painful movements or postures. Dystonia can be classified according to age of onset, bodily distribution of symptoms, and cause. Age of onset can occur during childhood or during adulthood. Dystonia can affect certain portions of the body (focal dystonia and multifocal dystonia) or the entire body (generalized dystonia). Torticollis is an example of a focal dystonia. Primary dystonia is defined when dystonia is the only symptom not associated with other pathology. Treatment options for dystonia include oral or injectable medications (i.e., botulinum toxin) and destructive surgical or neurosurgical interventions (i.e., thalamotomies or pallidotomyies) when conservative therapies fail.
In addition, DBS has been recently investigated in patients with chronic cluster headaches. Cluster headaches occur as episodic attacks of severe pain lasting from 30 minutes to several hours. The pain is usually unilateral and localized to the eye, temple, forehead, and side of the face. Autonomic symptoms that occur with cluster headaches include ipsilateral facial sweating, flushing, tearing, and rhinorrhea. Cluster headaches occur primarily in men and have been classified as vascular headaches that have been associated with high blood pressure, smoking, alcohol use, etc. However, the exact pathogenesis of cluster headaches is uncertain. Positron emission tomography (PET) scanning and magnetic resonance imaging (MRI) have shown the hypothalamic region may be important in the pathogenesis of cluster headaches. Alterations in hormonal/serotonergic function may also play a role. Treatment of cluster headaches includes pharmacologic interventions for acute episodes and prophylaxis, sphenopalatine ganglion (SPG) blockade, and surgical procedures such as percutaneous SPG radiofrequency rhizotomy and gamma knife radiosurgery of the trigeminal nerve.
DBS involves the stereotactic placement of an electrode into the brain (i.e., thalamus, globus pallidus, or subthalamic nucleus). The electrode is initially attached to a temporary transcutaneous cable for short-term stimulation to validate treatment effectiveness. Several days later, the patient returns to surgery for permanent subcutaneous implantation of the cable and a radiofrequency-coupled or battery-powered programmable stimulator. The electrode is typically implanted unilaterally on the side corresponding to the most severe symptoms. However, the use of bilateral stimulation using two electrode arrays has also been investigated in patients with bilateral, severe symptoms.
After implantation, noninvasive programming of the neurostimulator can be adjusted to the patient's symptoms. This feature may be important for patients with PD, whose disease may progress over time, requiring different neurostimulation parameters. Setting the optimal neurostimulation parameters may involve the balance between optimal symptom control and appearance of side effects of neurostimulation, such as dysarthria, disequilibrium, or involuntary movements.
The U.S. Food and Drug Administration (FDA) has approved the Activa® Tremor Control System, manufactured by Medtronic Corporation, MN for DBS. While the original 1997 FDA-labeled indications were limited to unilateral implantation of the device for the treatment of tremor, in January 2002, the FDA-labeled indications were expanded to include bilateral implantation as a treatment to decrease the symptoms of advanced Parkinson’s that are not controlled by medication. In April 2003, the labeled indications were expanded to include “unilateral or bilateral stimulation of the internal globus pallidus or subthalamic nucleus to aid in the management of chronic, intractable (drug refractory) primary dystonia, including generalized and/or segmental dystonia, hemidystonia and cervical dystonia (torticollis) in patients seven years of age or above.” This latter indication received FDA approval through the Humanitarian Device Exemption process. The Activa Tremor Control System consists of the following components: the implantable pulse generator, the deep brain stimulator lead, an extension that connects the lead to the power source, a console programmer, a software cartridge to set electrical parameters for simulation, and a patient control magnet, which allows the patient to turn the pulse generator on and off, or change between high and low settings.
This policy on unilateral DBS as a treatment for tremor is based on a 1997 Blue Cross Blue Shield Association Technology Evaluation Center (TEC) Assessment, and a 2001 TEC Assessment that focused on the use of deep brain stimulation of the globus pallidus and subthalamic nucleus for a broader range of Parkinson symptoms. The observations and conclusions of the TEC Assessment are summarized here. Articles published since these two assessments continue to report positive outcomes for deep brain stimulation for tremor and Parkinson disease.
Unilateral Deep Brain Stimulation of the Thalamus for Tremor
Unilateral or Bilateral Stimulation of the Globus Pallidus or Subthalamic Nucleus for Parkinson Symptoms
Deep Brain Stimulation for the Treatment of Dystonia
Deep brain stimulation for the treatment of primary dystonia received FDA approval through the Humanitarian Device Exemption (HDE) process. The HDE approval process is available for conditions that affect less than 4,000 Americans per year. According to this approval process, the manufacturer is not required to provide definitive evidence of efficacy, but only probable benefit. The approval was based on the results of DBS in 201 patients represented in 34 manuscripts. There were three studies that reported at least ten cases of primary dystonia. In these studies, clinical improvement ranged from 50% to 88%. A total of 21 pediatric patients were studied; 81% were older than seven years. Among these patients there was about a 60% improvement in clinical scores. As noted in the analysis of risk and probably benefit, the only other treatment options for chronic refractory primary dystonia are neuro destructive procedures. DBS provides a reversible alternative. The FDA Summary of Safety and Probable Benefit states, “Although there are a number of serious adverse events experienced by patients treated with deep brain stimulation, in the absence of therapy, chronic intractable dystonia can be very disabling and, in some cases, progress to a life-threatening stage or constitute a major fixed handicap. When the age of dystonia occurs prior to the individual reaching their full adult size, the disease not only can affect normal psychosocial development but also cause irreparable damage to the skeletal system. As the body of the individual is contorted by the disease, the skeleton may be placed under constant severe stresses that may cause permanent disfigurement. Risks associated with deep brain stimulation for dystonia appear to be similar to the risk associated with the performance of stereotactic surgery and the implantation of deep brain stimulation systems for currently approved indications, except when used in either child or adolescent patient groups.”
Since the FDA approval, there have been additional published trials of DBS for dystonia, which continue to report positive results. Vidailhet and colleagues reported the results of a prospective multi-institutional case series of 22 patients with primary generalized dystonia. Symptoms were evaluated prior to surgery and at several points up to one year of follow-up, in a double-blind fashion with the stimulator turned on and off. Dystonia scores were significantly better with the neurostimulator turned on.
Deep Brain Stimulation for the Treatment of Headaches
DBS the posterior hypothalamus for the treatment of chronic cluster headaches has been investigated. Recent functional studies have suggested cluster headaches have a central hypothalamic pathogenesis. Franzini and colleagues and Leone et al, reported deep brain stimulation with long-term, high-frequency, electrical stimulation of the ipsilateral posterior hypothalamus resulted in long-term pain relief without significant adverse effects in those patients with chronic cluster headaches. The results from these reports seem promising; however, the authors note further studies are needed to determine the long-term safety and effectiveness of this treatment.
A systematic review of 34 studies (921 patients) examined outcomes following subthalamic stimulation for patients with Parkinson’s disease who had failed medical management (e.g., motor fluctuations, dyskinesia, and other medication side effects). Twenty studies, primarily class IV (uncontrolled cohorts or case series), were included in the meta-analysis. Subthalamic stimulation was found to improve activities of daily living by 50% over baseline as measured by the Unified Parkinson’s Disease Rating Scale (UPDRS) part II (decrease of 13.35 points out of 52). There was a 28-point decrease in the UPDRS III score (out of 108), indicating a 52% improvement in the severity of motor symptoms while the patient was not taking medication. A strong relationship was found between the pre-operative dose response to L-dopa and improvements in both the UPDRS II and III. The analysis found a 56% reduction in medication use, a 69% reduction in dyskinesia, and a 35% improvement in quality of life with subthalamic stimulation.
Two randomized trials assessed the efficacy of subthalamic stimulation for Parkinson’s disease. The German Parkinson Study Group randomized 78 patient pairs with advanced Parkinson’s disease and severe motor symptoms to either subthalamic stimulation or medical management. Subthalamic stimulation improved severity of symptoms without medication in 55 of 78 pairs (from 48 to 28 on the UPDRS III). Improvements in quality of life were greater than medical management in 50 of 78 pairs (average change from 42 to 32 on the 100-point Parkinson’s Disease Questionnaire), with 24% to 38% improvements in subscales for mobility, activities of daily living, emotional well-being, stigma, and bodily discomfort. Serious adverse events were more common with neurostimulation (13% vs. 4%) and included a fatal intracerebral hemorrhage. Another European multicenter study assessed whether subthalamic stimulation might maintain quality of life and motor function if performed earlier in the course of the disease. Ten matched patient pairs younger than 55 years of age with mild to moderate motor signs were randomly assigned to DBS or medical management. There was no difference in the severity of parkinsonian motor disability while receiving medication. However, in the medically treated patients both the daily dose of levodopa and the severity of levodopa-induced motor complications increased over the 18 months of the study (12% and 15%, respectively), while in the surgical patients the daily dose of levodopa was reduced by 57% and the severity of levodopa-induced motor complications improved by 83%. Additional studies are needed to determine the long-term effect of subthalamic stimulation in this younger patient population.
The Deep-Brain Stimulation for Dystonia Study Group compared bilateral pallidal neurostimulation with sham stimulation in 40 patients with dystonia who had failed medical management (three-month randomized trial with a six-month open-label extension). Blinded assessment with the Burke-Fahn-Marsden Dystonia Rating Scale found improvements in the movement score (16 points vs. 1.6 points in sham controls), which corresponded to a 39% reduction in symptoms. Disability scores improved by four points in the neurostimulation group compared with a 0.8-point improvement in the control subjects (38% improvement). The study found a 30% improvement in quality of life (change of 10 vs. 4 points in controls) following stimulation of the globus pallidus. There was high variability in baseline scores and in the magnitude of improvement; six patients (17%) were considered to have failed treatment (< 25% improvement), five patients (25%) improved by more than 75%. No single factor was found to predict the response to treatment. Independent assessors found similar improvements in the control group after the six-month open-label extension.
Stimulation of the globus pallidus has also been examined as a treatment of tardive dyskinesia in a phase II double-blinded (presence and absence of stimulation) multicenter study. The trial was stopped early due to successful treatment (greater than 40% improvement) in the first 10 patients. Additional studies with more patients and longer follow-up are needed. Prospective, controlled trials are lacking for other disorders. Stimulation of the posterior hypothalamus was reported to have completely resolved headache in 10 of 16 chronic cluster headache patients and in one patient with neuralgiform headache; treatment failed in three of three patients who had atypical facial pain. In addition to the areas of research discussed above, deep brain stimulation is being investigated for the treatment of Tourette syndrome, depression, obsessive compulsive disorder, and epilepsy. Evidence remains insufficient to evaluate the efficacy of DBS for these disorders.
This policy was updated with a MEDLINE® search conducted in June 2009. Schuurman and colleagues followed 65 patients comparing thalamic stimulation and thalamotomy for treatment of tremor due to PD (45 patients), essential tremor (ET) (13 patients), and MS (10 patients). After five years, 48 patients were available for follow-up: 32 with PD, 10 with ET, and six with MS. The primary outcome measure was functional status on the Frenchay Activities Index (FAI); secondary measures were tremor severity, frequency of complications, and patients’ assessment of outcome. The mean difference in FAI scores was 4.4 (95% CI: 1.1–7.7) after six months, 3.3 (95% CI: -0.03–6.6) after two years and 4.0 (95% CI: 0.3–7.7) after five years in favor of stimulation. Tremor suppression was equally effective after both procedures, and stable in PD patients. A diminished effect was observed in half of the patients with ET and MS. Small numbers of patients with ET and MS limit conclusions with respect to these conditions. Neurological adverse effects were higher after thalamotomy. Subjective assessments favored stimulation. Hariz et al. evaluated outcomes of thalamic deep brain stimulation in patients with tremor predominant PD who participated in a multicenter European study and reported that, at six years post-surgery, tremor was still effectively controlled and appendicular rigidity and akinesia remained stable when compared with baseline.
Weaver and colleagues report six-month outcomes of a multicenter randomized, controlled trial comparing DBS with best medical therapy for patients with advanced PD. Of 278 patients that were screened, 255 were randomized; 134 to best medical therapy and 121 to DBS (61 to stimulation of the globus pallidus and 60 to stimulation of the subthalamic nucleus). By intention-to-treat analysis, patients who received DBS gained a mean of 4.6 hours a day of on time without troubling dyskinesia compared to no hours gained for patients receiving best medical therapy (p<0.001). Seventy-one percent of DBS patients experienced clinically meaningful motor function improvements (i.e., >5 point change in Unified Parkinson Disease Rating Scale of motor function) versus 32% of best medical therapy group. Significantly greater improvements in quality of life measures were achieved by DBS patients. At least one serious adverse event occurred in 49 DBS patients versus 15 in the best medical therapy patients, including 39 related to the surgical procedure and one death secondary to cerebral hemorrhage.
Witt et al. performed an ancillary protocol as part of a multicenter randomized, controlled trial to assess neuropsychiatric consequences of DBS in patients with Parkinson’s disease. One hundred-twenty-three patients with PD and motor fluctuations were randomized to DBS or best medical treatment. Neuropsychological and psychiatric examinations at baseline and six months post-implantation were compared. DBS of the subthalamic nucleus did not reduce overall cognition or affectivity. There was a selective decrease in frontal cognitive functions and an improvement in anxiety in patients after treatment that did not affect improvements in quality of life.
Appleby et al. report on a meta-analysis focused on adverse events associated with DBS in order to assess the risks and benefits of the treatment as they relate to its potential use in the psychiatric setting. They concluded that DBS is an effective treatment for PD, dystonia, and essential tremor and rates of depression, cognitive impairment, mania, and behavior change are low. Prevalence of depression was 2–4%; mania 0.9–1.7%, emotional changes 0.1–0.2%, and suicidal ideation or suicide attempt was 0.3–0.7%. The completed suicide rate was 0.16–0.32%. In light of the rate of suicide in patients treated with DBS, particularly with thalamic and globus pallidus interna (GPi) stimulation, the authors argue for prescreening patients for suicide risk.
A number of recent papers, mainly case series, focus on the use of DBS for treatment of dystonia. Vidailhet et al. compared outcomes at three years with those reported at one year for the 22 patients in their study of bilateral, pallidal DBS for generalized dystonia referenced in a previous update and found that the motor improvement observed at one year was maintained. At three years, measures of cognition and mood were unchanged from baseline and one year evaluations. Egidi et al. retrospectively reviewed records of 69 patients treated in multiple Italian centers with DBS implanted in the GPi; 37 patients had primary and 32 had secondary dystonia. Improvement of at least 50% in Burke-Fahn-Marsden severity scale was reached by 45% of primary and 37% of secondary dystonia patients at 3–84 months’ follow-up (longer than 24 months in half of the patients).
Other Neurological Applications
No controlled trials of DBS for seizures were identified. A multicenter, randomized controlled trial of stimulation of the anterior nucleus of the thalamus in epilepsy (SANTE) is in progress. Two small cross-over studies of DBS for Tourette syndrome were identified, one comparing unilateral and bilateral stimulation (five patients) and the other with three patients comparing thalamic, pallidal, simultaneous thalamic and pallidal, and sham stimulation. No controlled trials of DBS for tardive dyskinesia or cluster headache were found.
A crossover, double-blind, multicenter study of DBS for treatment of refractory obsessive-compulsive disorder (OCD) is reported by Mallet et al. Eighteen patients were enrolled, one withdrew and one required removal of the stimulator before randomization because of infection. Three months after surgery, eight patients were randomly assigned to receive active stimulation for three months, followed by one month of washout, then three months of sham stimulation (on-off group). The other group followed the same treatment schedule in reverse (off-on group). New or worsening symptoms were classified as adverse events. It was recommended that medical treatment remain stable and adjustments necessitated by the patient’s psychiatric condition were recorded. Medication was held constant during the 10-month protocol, except for transient increase in benzodiazepine therapy in three patients and augmentation of neuroleptic treatment in one patient for exacerbated anxiety. The primary outcome measure was severity of OCD as assessed by the Yale-Brown Obsessive Compulsive Scale (Y-BOCS) measured at the end of each period. The Y-BOCS score was significantly lower at the end of active stimulation than at the end of the sham stimulation (mean score, 19 +/- 8 vs. 28 +/- 7; p=0.01) independent of the group and the period. No significant carryover effect between treatment phases was detected. Patients who had active stimulation first (on-off group) tended to have a larger treatment effect than the off-on group (p=0.06).
Outcomes on secondary measures of global health and functioning were significantly better at the end of the stimulation period. Scores on Montgomery and Asberg Depression Scale (MADRS), Brief Scale for Anxiety, neuropsychological ratings, and self-reported disability (Sheehan Disability Scale) did not differ significantly at the end of treatment and sham sessions. Fifteen serious adverse events were reported in 11 patients, the most serious a parenchymal brain hemorrhage. Transient motor and psychiatric symptoms induced by active stimulation resolved spontaneously or with adjustment of stimulation settings. Seven behavioral adverse events were reported in five patients during stimulation. Hypomania was the main psychiatric serious adverse event; symptoms resolved with adjustment of stimulation settings. The authors note that the multicenter design might be a limitation of the study because of variation in targeting of stimulation. In addition, in order to preserve blinding, stimulation settings were kept below the threshold known to induce adverse effects and may have been too low to reduce symptoms. They conclude that their finding suggest that DBS may lessen severity of symptoms; however, serious adverse events did occur. Larger studies with longer follow-up are needed including evaluation of quality of life and ability to function in social and work situations.
Sachdev and Chen note in a January 2009 review that there has been a shift of interest in psychosurgery away from ablative techniques and toward deep brain stimulation. Studies of DBS for depression and obsessive compulsive disorder, however, are few and involve small numbers of subjects and “more data are needed on technical details and outcomes before the possible therapeutic role of DBS can be established.”
In summary, these multiple recent publications support current policy; they also reflect interest in DBS as a potential treatment for a growing number of additional clinical indications.
In February 2009, the FDA approved deep brain stimulation with the Reclaim device (Medtronic, Inc.) via the Humanitarian Device Exemption (HDE) process for the treatment of severe obsessive-compulsive disorder (OCD).
A search of peer reviewed literature through June 2009 identified any additional information that would change the coverage position of this medical policy.
Each benefit plan, summary plan description or contract defines which services are covered, which services are excluded, and which services are subject to dollar caps or other limitations, conditions or exclusions. Members and their providers have the responsibility for consulting the member's benefit plan, summary plan description or contract to determine if there are any exclusions or other benefit limitations applicable to this service or supply. If there is a discrepancy between a Medical Policy and a member's benefit plan, summary plan description or contract, the benefit plan, summary plan description or contract will govern.
The coding for deep brain stimulation consists of a series of codes describing the various steps of the procedure;
Implantation of Electrodes: If a patient is undergoing a bilateral electrode arrays, this code may be used twice. In some instances, patients undergo bilateral implantation in a staged procedure.
Electronic Analysis: Over time, patients may undergo several sessions of electronic analysis and programming to find the optimal programming parameters.
The information contained in this section is for informational purposes only. HCSC makes no representation as to the accuracy of this information. It is not to be used for claims adjudication for HCSC Plans.
The Centers for Medicare and Medicaid Services (CMS) does have a national Medicare coverage position.
A national coverage position for Medicare may have been developed or changed since this medical policy document was written. See Medicare's National Coverage at <http://www.cms.hhs.gov>.
Deep Brain Stimulation of the Thalamus for Tremor. Chicago, Illinois: Blue Cross Blue Shield Association – Technology Evaluation Center Assessment Program. (1997 December) 12(20):1-29.
Bilateral DBS of the Subthalamic Nucleus or the Globus Pallidus Interna for Treatment of Advanced Parkinson’s disease. Chicago, Illinois: Blue Cross Blue Shield Association – Technology Evaluation Assessment Program. (2002 February) 16(16):1-72.
FDA – Summary of Safety and Probably Benefit, Medtronic Activa Dystonia Therapy™. Federal Drug Administration – Center for Devices and Radiologic Health (2003 April 15) Available at <http://www.fda.gov>.
Franzini, A., Ferroli, P., et al. Stimulation of the posterior hypothalamus for treatment of chronic intractable cluster headaches: first reported series. Neurosurgery (2003) 52(5):1095-101.
Leone, M., May, A., et al. Deep brain stimulation for intractable chronic cluster headache: proposals for patient selection. Cephalalgia (2004) 24(11):934-7.
Franzini, A., Ferroli, P., et al. Hypothalamic deep brain stimulation for the treatment of chronic cluster headaches: a series report. Neuromodulation (2004) 7(1):1-8.
Halbig, T.D., Gruber, D., et al. Pallidal stimulation in dystonia: effects on cognition, mood, and quality of life. Journal of Neurology, Neurosurgery and Psychiatry (2005) 76(12):1713-6.
Vidailhet, M., Vercueil, L., et al. Bilateral deep-brain stimulation of the globus pallidus in primary generalized dystonia. New England Journal of Medicine (2005) 352(5):459-67.
Deep Brain Stimulation. Chicago, Illinois: Blue Cross Blue Shield Association Medical Policy Manual (2006 March) Surgery 7.01.63.
Kleiner-Fisman, G., Herzog, J., et al. Subthalamic nucleus deep brain stimulation: summary and meta-analysis of outcomes. Mov Disord (2006) 21(supplement 14):S290-304.
Deuschl, G., Schade-Brittinger, C., et al. German Parkinson Study Group, Neurostimulation Section. A randomized trial of deep-brain stimulation for Parkinson's disease. New England Journal of Medicine (2006) 355(9):896-908.
Kupsch, A., Benecke, R., et al. Deep-Brain Stimulation for Dystonia Study Group. Pallidal deep-brain stimulation in primary generalized or segmental dystonia. New England Journal of Medicine (2006) 355(19):1978-90.
Damier, P., Thobois, S., et al. French Stimulation for Tardive Dyskinesia (STARDYS) Study Group. Bilateral deep brain stimulation of the globus pallidus to treat tardive dyskinesia. Archive of General Psychiatry (2007) 64(2):170-6.
Schupbach, W.M., Maltete, D., et al. Neurosurgery at an earlier stage of Parkinson disease: a randomized, controlled trial. Neurology (2007) 68(4):267-71.
Broggi, G., Franzini, A., et al. Update on neurosurgical treatment of chronic trigeminal autonomic cephalalgias and atypical facial pain with deep brain stimulation of posterior hypothalamus: results and comments. Neurology and Science (2007) 28(supplement 2):S138-45.
<www.ClinicalTrials.gov> (accessed – 06/23/2009).
Schuurman, P.R., Bosch, D.A., et al. Long-term follow-up of thalamic stimulation versus thalamotomy for tremor suppression. Movement Disorders (2008) 23(8):1146-53.
Hariz, M.I., Krack, P., et al. Multicentre European study of thalamic stimulation for parkinsonian tremor: a 6 year follow-up. Journal of Neurology and Neurosurgical Psychiatry (2008) 79(6):694-9.
Weaver, F.M., Follett, K., et al. Bilateral deep brain stimulation vs. best medical therapy for patients with advanced Parkinson disease. JAMA (2009) 301(1):63-73.
Appleby, B.S., Duggan, P.S., et al. Psychiatric and neuropsychiatric adverse events associated with deep brain stimulation: a meta-analysis of ten years’ experience. Movement Disorders (2007) 22(12):1722-8.
Vidailhet, M., Vercueil, L., et al. Bilateral, pallidal, deep-brain stimulation in primary generalized dystonia: a prospective 3 year follow-up study. Lancet Neurology (2007) 6(3):223-9.
Egidi, M., Franzini, A., et al. A survey of Italian cases of dystonia treated by deep brain stimulation. Journal of Neurosurgical Science (2007) 51(4):153-8.
Maciunas, R.J., Maddux, B.N., et al. Prospective randomized double-blind trial of bilateral thalamic deep brain stimulation in adults with Tourette syndrome. Journal of Neurosurgery (2007) 107(5):1004-14.
Welter, M.L., Mallet, L., et al. Internal pallidal and thalamic stimulation in patients with Tourette syndrome. Archives of Neurology (2008) 65(7):952-7.
Mallet, L., Polosan, M., et al. Subthalamic nucleus stimulation in severe obsessive-compulsive disorder. New England Journal of Medicine (2008) 359(20):2121-34.
Witt, K., Daniels, C., et al. Neuropsychological and psychiatric changes after deep brain stimulation for Parkinson’s disease: a randomized, multicentre study. Lancet Neurology (2008) 7(7):605-14.
Sachdev, P.S., and X., Chen. Neurosurgical treatment of mood disorders: traditional psychosurgery and the advent of deep brain stimulation. Current Opinions in Psychiatry (2009) 22(1):25-31.
Deep Brain Stimulation. Chicago, Illinois: Blue Cross Blue Shield Association Medical Policy Manual. Surgery (2009 February) 7.01.63.
8/15/2009 Revised and updated entire document with literature search and no coverage change. This policy is no longer scheduled for routine literature review and update.
7/1/2009 CPT/HCPCS code(s) updated
5/1/2008 CPT/HCPCS code(s) updated
12/2007 CPT/HCPCS code(s) updated
9/1/2007 Revised/Updated Entire Document
1/1/2006 Codes Revised/Added/Deleted
5/15/2005 Revised/Updated Entire Document
11/2004 Codes Revised/Added/Deleted
2/2002 Codes Revised/Added/Deleted
11/2000 New Medical Document
|Title:||Effective Date:||End Date:|
|Deep Brain Stimulation (DBS)||08-15-2017||06-14-2018|
|Deep Brain Stimulation (DBS)||12-01-2016||08-14-2017|
|Deep Brain Stimulation||06-01-2015||11-30-2016|
|Deep Brain Stimulation for Tremor||06-01-2011||05-31-2015|
|Deep Brain Stimulation for Tremor||08-15-2009||05-31-2011|
|Deep Brain Stimulation for Tremor||05-01-2008||08-14-2009|
|Deep Brain Stimulation for Tremor||09-01-2007||04-30-2008|
|Deep Brain Stimulation for Tremor||05-15-2005||08-31-2007|
|Deep Brain Stimulation for Tremor||11-01-2000||05-14-2005|