Medical Policy


Subject:  Vagus Nerve Stimulation
Policy #:  SURG.00007Current Effective Date:  01/01/2014
Status:RevisedLast Review Date:  08/08/2013

Description/Scope

Vagus nerve stimulation (VNS) involves the use of a pulse generator, similar to a pacemaker, that is surgically implanted under the skin of the chest with an electrical lead (wire) connected from the generator to the left vagus nerve. Electrical signals are sent from the battery-powered generator to the vagus nerve via the lead. These signals are in turn sent to the brain.

This document addresses the use of an implantable VNS device and the electronic analysis of the implanted neurostimulator pulse generator system for the treatment of medically and surgically refractory seizures associated with intractable epilepsy and as a treatment of other conditions.

Position Statement

Medically Necessary:

Implantation of a vagus nerve stimulation device is considered medically necessary in an individual with medically and surgically refractory seizures as evidenced by:

Electronic analysis of an implanted neurostimulator pulse generator system for vagus nerve stimulation is considered medically necessary when the implantation occurred because the above criteria were met.

Investigational and Not Medically Necessary:

Implantation of a vagus nerve stimulation device is considered investigational and not medically necessary as a treatment for all other conditions, including, but not limited to:

Electronic analysis of an implanted neurostimulator pulse generator system for vagus nerve stimulation is considered investigational and not medically necessary when the medically necessary criteria for device implantation are not met.

Rationale

VNS as Treatment of Medically and Surgically Refractory Seizures

Published evidence from well-designed multimember trials involving over 300 participants with long-term follow-up demonstrates the use of VNS as an adjunct to optimal use of antiepileptic drugs in the treatment of medically refractory individuals with at least six partial onset seizures per month reduces seizure frequency by approximately 25% after three months of treatment (Morris, 1999; Murphy, 1999). In individuals who achieve an initial reduction in seizure frequency, the beneficial treatment effect appears to be maintained and may increase with time. Adverse effects are mild and consist primarily of hoarseness or voice change during periods of stimulation. With increasing experience with VNS, candidate selection is not based on the number of seizures alone, but on the presence of seizures that are refractory to medical therapy, either in terms of persistence of seizures, or due to intolerable side effects of drug therapy (Benbadis, 2000; Fisher, 1999). Additionally, the original FDA approval limited the use of VNS to individuals over the age of 12 years. Initial studies reported results that support the safety of the device in children with refractory seizures (Patwardhan, 2000; Salinsky, 1996). The long-term efficacy and safety of VNS therapy in the pediatric population was further reported in several moderately large retrospective case series (Alexopoulos, 2006; Benifla, 2006; De Herdt, 2007). Tecoma and Iragui (2006) observed that since approval of VNS for partial seizures, a number of case series including individuals with generalized seizures have been published. These series report seizure reduction rates similar or greater than those reported in partial epilepsy, and note that "this body of evidence suggests that VNS has broad antiepileptic efficacy." The authors suggest that these results may be particularly important since resective epilepsy surgery is generally not feasible in these individuals. You and colleagues (2007) reported that 15 of 28 children (53.6%) with refractory seizures showed a greater than 50% reduction in seizure frequency, nine children (32%) had a greater than 75% reduction, and there were no significant differences when groups were compared by seizure type or etiology. Tecoma and Iragui (2006) cite a multicenter retrospective analysis of 50 children with Lennox-Gastaut syndrome (LGS) treated with VNS. Median seizure reduction at six months was 88% for tonic seizures and 81% for atypical absences. You and colleagues (2008) compared VNS and total corpus callosotomy for LGS. Of the 14 individuals who underwent a corpus callosotomy, nine individuals (64%) had a greater than 50% reduction in seizure frequency and five individuals (36%) had a greater than 75% reduction. Of the 10 individuals who underwent VNS implantation, seven individuals (70%) had a greater than 50% reduction in seizure frequency and two individuals (20%) had a greater than 75% reduction.

An observational study by Kostov and colleagues (2009) investigated the utility of long-term VNS therapy in 30 individuals with LGS (median observation time was 52 months). The authors reported a median reduction in the total number of seizures and different seizure types was 60.6%. Seizure reduction of 61% was also reported in a case series of 12 individuals with drug-resistant idiopathic generalized epilepsy (Kostov, 2007). Based on these data, the conclusion can be drawn that VNS is an effective treatment for refractory seizures other than partial epilepsy.

Additional retrospective case series measuring the long term effects of VNS for medically and surgically refractory seizures in adults and the pediatric population have subsequently been published in the peer-reviewed literature. Significant reductions in seizure frequency with possible cumulative effect have been reported along with a reduction in surgical complications and untoward side effects with chronic VNS therapy (Coykendall, 2010; Elliott, 2011a; Elliott, 2011b; Elliott, 2011c; Ghaemi, 2010; Kabir, 2009; Siddiqui, 2010; Vale, 2011). Englot and colleagues (2011) performed the first meta-analysis of VNS efficacy in epilepsy, identifying 74 clinical studies with 3321 participants with intractable epilepsy. These studies included three blinded, randomized controlled trials (Class I evidence); two nonblinded, randomized controlled trials (Class II evidence); 10 prospective studies (Class III evidence); and numerous retrospective studies. After VNS implantation, seizure frequency was reduced by an average of 45%, with a 36% reduction in seizures at 3-12 months after surgery and a 51% reduction after greater than one year of therapy. At the last follow-up, seizures were reduced by 50% or more in approximately 50% of the individuals, and VNS predicted an equal to or greater than 50% reduction in seizures (main effects, odds ratio of 1.83; 95% confidence interval 1.80-1.86). Individuals with generalized epilepsy and children benefited significantly from VNS despite their exclusion from initial approval of the device. The authors concluded that VNS is an effective and relatively safe adjunctive therapy in individuals with medically refractory epilepsy not amenable to resection. However, it is important to recognize that complete seizure freedom is rarely achieved using VNS and that a quarter of individuals do not receive any benefit from therapy.

VNS as Treatment of Refractory Depression

Interest in the application of VNS for treatment of refractory depression is related to reports of improvement in depressed mood among individuals with epilepsy undergoing VNS. In 2005, the vagus nerve stimulator received U.S. Food and Drug Administration (FDA) approval for this indication. The data presented to the FDA by the manufacturer of the VNS Therapy® (Cyberonics, Inc., Houston, TX, U.S.A.) consisted of a case series of 60 individuals receiving VNS (Study D-01), a short-term (3-month) randomized sham-controlled clinical trial of 221 individuals (Study D-02), and an observational study comparing 205 individuals on VNS therapy to 124 individuals receiving ongoing treatment for depression (Study D-04) (George, 2005; Rush, 2000). Individuals who responded to sham treatment in the short-term randomized, controlled trial (approximately 10%) were excluded from the long-term observational study.

The primary efficacy outcome of interest is the relief of depression symptoms. This outcome may be assessed by any one of many different depression symptom rating scales. A 50% reduction from baseline score is considered to be a reasonable measure of treatment response. An improvement in depression symptoms may allow reduction of pharmacologic therapy for depression, with a reduction in side effects related to that form of treatment. In the studies evaluating VNS therapy, the four most common instruments used were the Hamilton Rating Scale for Depression (HAMD), Clinical Global Impression, Montgomery and Åsberg Depression Rating Scale (MADRS), and the Inventory of Depressive Symptomatology Self-Related (IDS-SR).

The case series data reported rates of improvement, as measured by a 50% improvement in depression score of 31% at 10 weeks to greater than 40% at one to two years. This appeared to stabilize out to two years, but there were substantial losses to follow-up (n=42 at two years versus original sample of 59) (Marangell, 2002; Rush, 2000; Sackeim, 2001). Natural history, placebo effects, and the expectations of the individual and their medical practitioner make it difficult to infer efficacy from this case series data.

The D-02 randomized trial (Rush, 2000; Rush, 2005a) comparing VNS therapy to a sham control, (implanted but inactivated VNS), showed a non-statistically significant result for the principal outcome at three months. Fifteen percent of VNS subjects responded, versus 10% of control subjects (p=0.31). The IDS-SR was considered a secondary outcome, showing a difference that was statistically significant in favor of VNS (17.4% versus 7.5%, p=0.04). All other outcomes assessed in the trial did not show statistically significant differences between groups.

The observational study comparing subjects participating in the randomized clinical trial and a separately recruited control group (D-04 vs. D-02) evaluated VNS therapy out to one year, showing a statistically significant difference in the rate of change of depression score (p<0.001) (George 2005; Rush, 2000). This study was conceived after the results of the randomized clinical trial were known. The outcomes of this study, however, may have been confounded by issues such as unmeasured differences between subjects, nonconcurrent controls, differences in sites of care between subjects with VNS therapy and controls, and differences on concomitant therapy changes. Analyses performed on subsets of subjects cared for in the same sites and censoring observations after treatment changes, generally showed diminished differences in apparent treatment effectiveness of VNS with almost no statistically significant differences. Considering these concerns about the quality of the observational data, these results lack strong evidence to support the effectiveness of VNS therapy as a treatment for refractory depression.

Nahas and colleagues (2005) evaluated the safety and effectiveness of VNS in an acute phase pilot study of 59 individuals with treatment-resistant major depressive episode (MDE). They examined the effects of adjunctive VNS over 24 months in this adult population. Adults treated in the outpatient setting with chronic or recurrent major depressive disorder or bipolar (I or II) disorder and experiencing a treatment-resistant, non-psychotic MDE (DSM-IV criteria) received two years of VNS. Changes in psychotropic medications and VNS stimulus parameters were allowed only after the first three months. Response was defined as greater than or equal to 50% reduction from the baseline 28-item Hamilton Rating Scale for Depression (HAMD-28) total score, and remission was defined as a HAMD-28 score less than or equal to 10. Based on last observation carried forward analyses, HAMD-28 response rates were 31% (18/59) after three months, 44% (26/59) after one year, and 42% (25/59) after two years of adjunctive VNS. Remission rates were 15% (9/59) at three months, 27% (16/59) at one year, and 22% (13/59) at two years. By two years, two deaths (unrelated to VNS) had occurred, four participants had withdrawn from the study, and 81% (48/59) were still receiving VNS. Longer-term VNS was generally well tolerated, however, at 24 months, the accumulated serious adverse events affected 42% of the individuals. These investigators concluded that their findings suggest that individuals with chronic or recurrent, treatment-resistant depression (TRD) may show long-term benefit when treated with VNS. However, the number of responders and the degree of their improvement waxed and waned over the two year study. Since there was no control group, it is difficult to determine if this was due to the VNS or the natural course of chronic depression. There was no information on whether any subjects failed to respond to either electroconvulsive therapy (ECT) or details about antidepressant augmentation strategies utilized prior to being accepted into this study.

A review of the literature indicates there continues to be a lack of randomized controlled studies conducted in the United States (U.S.) that report clinical outcomes on any new or different individuals than those reported on in prior studies. These studies involve the same data that was reanalyzed from prior studies and continued to demonstrate a lack of evidence of efficacy beyond that provided by the original data. In summary, the available evidence is insufficient to permit conclusions regarding the effect of VNS therapy on health outcomes or its effect compared with alternative therapies. Further randomized controlled trials are needed to address the complex and unresolved issues of dose, sham control, participant blinding, and length of treatment phase to demonstrate the efficacy of VNS as a treatment of depression (George, 2007).

An open-label, uncontrolled, unblinded study of VNS therapy, in addition to concomitant treatment with antidepressant medications (stable for four weeks prior to study entry, during the recovery period and the acute study phase), enrolled individuals with TRD or bipolar I or II disorder at nine European sites from 2001 to 2005 (D03) (Schlaepfer, 2008). This study was reported as being partially sponsored by the VNS device manufacturer. The study protocol was similar to the D01 study conducted in the U.S., except that: (1) the study inclusion required a score equal to or greater than 20 on the HAMD-24 scale in the D03 study, as opposed to equal to or greater than 20 on the HAMD-28 scale in the D01 study, (2) the maximum age at entry was 80 in the D03 study and 70 in the D01 study, and (3) the number of failed adequate medication trials was equal to or greater than two but less than six in the D03 study versus equal to or greater than two in the D01 study. During the long-term follow-up period, adjustments in stimulation parameters and medications were permitted. Of the 74 participants implanted with the device, four withdrew during the acute study period. Seven participants dropped out during the first-year long-term study period, five due to adverse events or lack of efficacy, and two participants committed suicide. Primary outcomes were reported as a reduction in the severity of depression as measured by the HAMD-24, but HAMD-28 was assessed and used for comparison of results to the D01 study. The baseline HAMD-28 score averaged 34. After three months of VNS, response rates (greater than or equal to 50% reduction in baseline scores) reached 37% and remission rates (HAMD-28 score less than 10) 17%. Response rates increased to 53% after one year of VNS, and remission rates reached 33%. Response was defined as sustained if no relapse occurred during the first year of VNS after response onset; 44% of participants met these criteria. Median time to response was nine months. Most frequent side-effects were voice alteration (63% at three months of stimulation) and coughing (23%). Comparing results of this study to the D01 study results, the investigators reported a decrease in severity of depression after three, six, nine, and 12 months compared to baseline HAMD-28 score, reaching significance in both samples over time, with higher efficacy in the D03 study compared to the D01 study. This was attributed to the lower measures of baseline depression in the D01 study. The investigators, however, reported "a major shortcoming" of this study, as in the U.S. D01 study, was that effectiveness was not assessed in a sham controlled design, "limiting interpretations on clinical utility." In addition, the authors suggest in future trials of VNS for depression, "it might therefore be valuable to study the specific characteristics of personality of a patient population with treatment resistance interested in this procedure (VNS) to judge whether personality features contribute differentially to treatment effects" (Schlaepfer, 2008).

Cristancho and colleagues (2011) followed participants with major depressive disorder (n=10) and with bipolar disorder (n=5) at 6 and 12 months post-VNS implantation between November 2005 and August 2006. At the 12 month follow-up, 4 of 15 participants responded and 1 of 15 participants remitted according to the principal response criteria. These outcomes are comparable to those observed in previous VNS efficacy studies and with a similar side effect profile, however, the small sample size, lack of a comparison group, and short-term outcome measurements limit this study in drawing conclusions concerning the net health benefit of VNS for this group of individuals.

Fitzgerald and Daskalakis stated in a 2008 review that "given the invasive nature of vagal nerve stimulation and potential side effects, further research is urgently required." A guideline statement from the Canadian Network for Mood and Anxiety Treatments included a review of the literature on VNS for depression and concluded that there is a lack of substantive evidence for short-term and long-term efficacy in acute severe depression, and that the appropriate place of VNS remains to be determined (Kennedy, 2009). A small open label, longitudinal cohort study by Bajbouj and colleagues (2010) reported data after following participants for two years. The results indicated that 53.1% (26/49) of individuals met the treatment response criteria (greater or equal to a 50% reduction in the HAMD-28 scores from baseline) and 38.9% (19/49) fulfilled the remission criteria (HAMD-28 scores less than or equal to 10) while on VNS. These results are limited in demonstrating improved health outcomes due to the small study population and lack of a comparison group.

A workgroup of the American Psychiatric Association has published the third edition of the Practice Guideline for the Treatment of Patients with Major Depressive Disorder. According to the guideline, "Vagus nerve stimulation is approved for use in patients with treatment-resistant depression on the basis of its potential benefit with long-term treatment. There is no indication for the use of VNS in acute phase treatment of depression, as data showed no evidence for acute efficacy" (Rush, 2005a; Sackeim, 2001). For individuals "whose symptoms have not responded adequately to medication, ECT remains the most effective form of therapy and should be considered." However, for those individuals with TRD, "Vagus nerve stimulation (VNS) may be an additional option for individuals who have not responded to at least four adequate trials of antidepressant treatment, including ECT" (Level of Clinical Confidence III:  May be recommended on the basis of individual circumstance) (Gelenberg/APA, 2010).

An Agency for Healthcare Research and Quality's (AHRQ) comparative effectiveness review (Gaynes, 2011) summarized the evidence concerning the effectiveness of four treatments in the clinical management of TRD, including ECT, repetitive transcranial magnetic stimulation (rTMS), VNS, and cognitive behavioral therapy (CBT) or interpersonal psychotherapy (IPT). The following is a summary of the findings on the efficacy and safety of VNS for adult TRD:

The review concluded that many clinical questions about efficacy and effectiveness remain unanswered. Comparative clinical research on nonpharmacologic interventions in a TRD population is in its infancy. Comparison of any of the potential interventions in the treatment of TRD, nonpharmacologic or otherwise, is hampered by variable definitions of TRD, heterogeneity of study participants, and lack of clinically meaningful interpretation of pertinent outcome measures as relevant studies did not assess both response and remission rates.

VNS as Treatment of Other Conditions

Unintended weight loss has been observed in participants in studies of VNS prompting interest in use of the technology to prevent or treat obesity. Bodenlos and colleagues (2007) investigated whether VNS might affect food cravings in individuals with chronic TRD. Thirty-three participants were divided into three groups; 11 subjects receiving VNS for depression, 11 subjects with depression but not receiving VNS, and 11 healthy controls. Most participants (42%) had a BMI in the normal range. Participants viewed food images on a computer in random order and then a second time in the same order, and were asked after each viewing how much they would like to eat each food if it were available and how well they would be able to resist tasting each one. VNS devices were turned on for one viewing and off for the other. The depression VNS group had greater differences in food cravings between viewings in the sweet food category than the other two groups. No significant differences between groups were found for foods in proteins and vegetables/fruits categories. A significant proportion of the variability in VNS–related changes in cravings for sweet foods was attributed to clinical VNS device settings, depression scores and BMI. A number of limitations in the study prevent drawing conclusions about the impact of VNS on eating behavior including small study size, selection and lack of randomization, heterogeneity of groups with respect to depression, BMI, and age. Comorbidities including anxiety and medical conditions and drugs that might influence food intake and cravings were not considered. Large, well-designed and executed controlled studies are needed to evaluate the impact of VNS on eating behavior and obesity.

A possible role of VNS therapy to affect pain perception was evaluated by Mauskop (2005) in five individuals with severe, refractory chronic cluster and migraine headaches. Cecchini and colleagues (2009) evaluated VNS in a small study of four individuals suffering from daily headaches and chronic migraine. These studies are too small to draw conclusions on the effects of VNS for the treatment of headache. Mathew (2009) reviewed the current and future treatments for chronic migraine headaches, stating that clinical trials indicate combination therapy may have a place in treating refractory chronic migraine, yet, well-controlled multicenter trials are needed.

In an open-label, phase II trial of VNS therapy utilizing the CardioFit® device (BioControl Medical, Yehud, Israel - New Hope, Minnesota) for chronic heart failure, De Ferrari and colleagues (2011) reported improvements in New York Heart Association (NYHA) class II-IV individuals (n=32) in measures of quality of life, six-minute walk test, and left ventricular ejection fraction (from 22±7 to 29±8%, p=0.003). An international multicenter randomized clinical trial (INOVATE-HF) assessing the safety and efficacy of the CardioFit System in symptomatic individuals with heart failure is currently recruiting participants (Hauptman, 2012). To date, the CardioFit device has not received FDA clearance for VNS therapy or any other indication.

VNS therapy has been investigated as a treatment for essential tremor (Handforth, 2003), enhancing cognitive deficits in Alzheimer's disease (Merrill, 2006), anxiety disorders, and bulimia. Other studies explore the potential use of VNS in the treatment of autism (Danielsson, 2008), fibromylagia (Lange, 2011), morbid/resistant obesity (Camilleri, 2008; Sarr, 2012), addictions, sleep disorders, narcolepsy, coma, and memory and learning deficits (Ansari, 2007). A search of the clinicaltrials.gov database identified studies in various phases investigating the effects of implantable VNS on cluster headaches, Crohn's disease, myocardial function in heart failure, enteroendocrine secretion and glucose metabolism in Type 2 diabetes-related obesity, rheumatoid arthritis, and recovery from minimally conscious or persistently vegetative states after traumatic brain injury (U.S. National Institutes of Health, 2013). To date, the FDA has not cleared the use of any type of implantable VNS device for these indications. Well-designed, randomized clinical trials with larger populations are needed to demonstrate the safety and efficacy of VNS therapy as a treatment for any of these conditions.

Background/Overview

According to the Epilepsy Foundation (2013), epilepsy affects three million people in the U.S. and includes more than 300,000 children under the age of 15. More than 90,000 young people in this group have seizures that cannot be adequately treated. The National Institute of Neurological Disorders and Stroke (NINDS, 2013) reports that 20% of persons with epilepsy experience intractable seizures (seizures that do not respond to treatment).

The American Association of Neurological Surgeons (AANS, 2013) currently classifies seizures to include two basic categories: primary generalized seizures and focal seizures (previously referred to as partial seizures). Classifying the type of seizure is important in the selection of appropriate antiepileptic drug treatment. Despite advances in the medical and surgical treatment of epilepsy, 25% to 50% of individuals with epilepsy experience breakthrough seizures or suffer from debilitating adverse effects of antiepileptic drugs.

The VNS device is an implantable stimulator similar to a cardiac pacemaker. The surgery consists of implanting the pacemaker-like generator under the skin in the left chest area. A nerve stimulation electrode is tunneled under the skin to the lower neck where it is placed around the left cervical vagus nerve. The neurologist, using an external programmer sets or resets the stimulation parameters of the device to deliver preprogrammed intermittent electrical pulses to the vagus nerve, which then transmits that stimulation to the brain to create widespread antiepileptic effects. Additionally, when an individual senses a seizure coming on, he/she can activate the system to deliver an additional dose of stimulation by passing a magnet over the area of the chest where the device is implanted. The device is powered by a lithium thionyl chloride battery that must be replaced every 1.5-5 years depending on the stimulation parameters. Adverse effects of VNS therapy included voice alteration, headache, neck pain, and cough, which are known from prior experience with VNS therapy for seizures.

A VNS device was originally approved by the FDA for the treatment of refractory epilepsy. In April 1999, the Centers for Medicare and Medicaid Services (CMS) issued a national coverage determination (NCD 160.18, effective for services performed on or after July 1, 1999) for VNS as an effective treatment for medically refractory partial onset seizures when surgery is not recommended or has failed. At the same time, CMS determined that VNS was not medically reasonable and necessary for resistant depression. On July 15, 2005, the FDA granted premarket approval to Cyberonics, Inc. for their VNS Therapy System for the adjunctive long-term treatment of chronic or recurrent depression for individuals 18 years of age or older who are experiencing a major depressive episode and have not had an adequate response to four or more antidepressant treatments. CMS subsequently initiated a national coverage analysis in follow-up to a request to reconsider resistant depression as an additional indication for VNS (CMS, 2007). After a review of the evidence, CMS concluded in a national non-coverage determination (effective May 4, 2007) that VNS is not reasonable and necessary for individuals with TRD. Ongoing studies of VNS are documented on the clinicaltrials.gov database including a registry for individuals with treatment-resistant depression.

Definitions

Focal seizure: A seizure that begins with an electrical discharge in a relatively small area (called the focus) of the brain; previously referred to as a partial or localization-related seizure. In most cases, the cause is unknown, but may be related to a brain infection, head injury, stroke, or a brain tumor.

Medically refractory seizures: Seizures that occur despite treatment with therapeutic levels of antiepileptic drugs or seizures that cannot be treated with therapeutic levels of antiepileptic drugs because of intolerable adverse side effects.

Refractory depression: A major depressive disorder that fails to demonstrate an adequate response to an adequate treatment trial of antidepressant medications (i.e. sufficient intensity of treatment for sufficient duration); also referred to as treatment-resistant depression (TRD). Potential factors contributing to apparent non-response include trial adequacy, individual compliance, differential diagnosis, and treatable comorbid conditions.

Vagus nerve: A nerve that controls both motor and sensory functions of the gastrointestinal tract, heart and larynx; also referred to as the 10th cranial nerve.

Coding

The following codes for treatments and procedures applicable to this document are included below for informational purposes.  Inclusion or exclusion of a procedure, diagnosis or device code(s) does not constitute or imply member coverage or provider reimbursement policy.  Please refer to the member's contract benefits in effect at the time of service to determine coverage or non-coverage of these services as it applies to an individual member.

When services may be Medically Necessary when specified as vagus nerve stimulator and criteria are met:

CPT 
61885Insertion or replacement of cranial neurostimulator pulse generator or receiver, direct or inductive coupling; with connection to a single electrode array
64553Percutaneous implantation of neurostimulator electrode array; cranial nerve
64568Incision for implantation of cranial nerve (eg, vagus nerve) neurostimulator electrode array and pulse generator
64569Revision or replacement of cranial nerve (eg, vagus nerve) neurostimulator electrode array, including connection to existing pulse generator
95974-95975Electronic analysis of implanted neurostimulator pulse generator system; complex cranial nerve neurostimulator pulse generator/transmitter, with intraoperative or subsequent programming, with or without nerve interface testing
  
HCPCS 
C1767Generator, neurostimulator (implantable), nonrechargeable
L8679Implantable neurostimulator, pulse generator, any type
L8680Implantable neurostimulator electrode, each
L8685Implantable neurostimulator pulse generator, single array, rechargeable, includes extension
L8686Implantable neurostimulator pulse generator, single array, nonrechargeable, includes extension
  
ICD-9 Procedure[For dates of service prior to 10/01/2014]
04.92Implantation or replacement of peripheral neurostimulator
  
ICD-9 Diagnosis[For dates of service prior to 10/01/2014]
345.00-345.91Epilepsy
  
ICD-10 Procedure[For dates of service on or after 10/01/2014]
00HE0MZInsertion of neurostimulator lead into cranial nerve, open approach
00HE3MZInsertion of neurostimulator lead into cranial nerve, percutaneous approach
00HE4MZInsertion of neurostimulator lead into cranial nerve, percutaneous endoscopic approach
  
ICD-10 Diagnosis[For dates of service on or after 10/01/2014]
G40.001-G40.919Epilepsy and recurrent seizures

When services are Investigational and Not Medically Necessary:

For the procedure codes listed above when specified as vagus nerve stimulator when criteria are not met or for all other diagnoses (including but not limited to those listed below), or when the code describes a procedure indicated in the Position Statement section as investigational and not medically necessary.

ICD-9 Diagnosis[For dates of service prior to 10/01/2014]
 All other diagnoses, including, but not limited to:
278.00-278.03Overweight and obesity
296.00-296.99Episodic mood disorders
298.0Depressive type psychosis
299.00-299.01Autistic disorder
307.51Bulimia nervosa
327.00-327.8Organic sleep disorders
331.0Alzheimer's disease
333.1Essential and other specified forms of tremor
339.00-339.02Cluster headaches
343.0-343.9Infantile cerebral palsy
346.00-346.93Migraine
347.00-347.11Cataplexy and narcolepsy
428.0-428.9Heart failure
783.6Polyphagia
  
ICD-10 Diagnosis[For dates of service on or after 10/01/2014]
 All other diagnoses, including, but not limited to:
E66.01-E66.9Overweight and obesity
F30.10-F39Mood (affective) disorders
F50.2Bulimia nervosa
F84.0Autistic disorder
G25.0-G25.2Essential and other specified forms of tremor
G30.0-G30.9Alzheimer's disease
G43.001-G43.919Migraine
G43.A0-G43.D1Migraine
G44.001-G44.029Cluster headaches
G47.00-G47.9Organic sleep disorders
G80.0-G80.9Cerebral palsy
I50.1-I50.9Heart failure
R63.2Polyphagia

When services are also Investigational and Not Medically Necessary:

CPT 
0312TVagus nerve blocking therapy (morbid obesity); laparoscopic implantation of neurostimulator electrode array, anterior and posterior vagal trunks adjacent to esophagogastric junction (EGJ), with implantation of pulse generator, includes programming
0313TVagus nerve blocking therapy (morbid obesity); laparoscopic revision or replacement of vagal trunk neurostimulator electrode array, including connection to existing pulse generator
0314TVagus nerve blocking therapy (morbid obesity); laparoscopic removal of vagal trunk neurostimulator electrode array and pulse generator
0315TVagus nerve blocking therapy (morbid obesity); removal of pulse generator
0316TVagus nerve blocking therapy (morbid obesity); replacement of pulse generator
0317TVagus nerve blocking therapy (morbid obesity); neurostimulator pulse generator electronic analysis, includes reprogramming when performed
  
ICD-9 Diagnosis[For dates of service prior to 10/01/2014]
 All diagnoses
  
ICD-10 Diagnosis[For dates of service on or after 10/01/2014]
 All diagnoses
References

Peer Reviewed Publications:

  1. Alexopoulos AV, Kotagal P, Loddenkemper T, et al. Long-term results with vagus nerve stimulation in children with pharmacoresistant epilepsy. Seizure. 2006; 15(7):491-503.
  2. Ansari S, Chaudhri K, Al Moutaery K. Vagus nerve stimulation: indications and limitations. Acta Neurochir Supp. 2007; 97(2):281-286.
  3. Bajbouj M, Merkl A, Schlaepfer TE, et al. Two-year outcome of vagus nerve stimulation in treatment-resistant depression. J Clin Psychopharmacol. 2010; 30(3):273-281.
  4. Benbadis SR, Tatum WO, Vale FL. When drugs don't work. An algorithmic approach to medically intractable epilepsy. Neurology. 2000; 55(12):1780-1784.
  5. Benifla M, Rutka JT, Logan W, Donner EJ. Vagal nerve stimulation for refractory epilepsy in children: indications and experience at The Hospital for Sick Children. Childs Nerv Syst. 2006; 22(8):1018-1026.
  6. Bodenlos JS, Kose S, Borckardt JJ, et al. Vagus nerve stimulation acutely alters food craving in adults with depression. Appetite. 2007; 48(2):145-153.
  7. Camilleri M, Toouli J, Herrera MF, et al. Selection of electrical algorithms to treat obesity with intermittent vagal block using an implantable medical device. Surg Obes Relat Dis. 2009; 5(2):224-229.
  8. Cecchini AP, Mea E, Tullo V, et al. Vagus nerve stimulation in drug-resistant daily chronic migraine with depression: preliminary data. Neurol Sci. 2009; 30(suppl 1):S101-104.
  9. Coykendall DS, Gauderer MW, Blouin RR, Morales A. Vagus nerve stimulation for the management of seizures in children: an 8-year experience. J Pediatr Surg. 2010; 45(7):1479-1483.
  10. Cristancho P, Cristancho MA, Baltuch GH, et al. Effectiveness and safety of vagus nerve stimulation for severe treatment-resistant major depression in clinical practice after FDA approval: outcomes at 1 year. J Clin Psychiatry. 2011; 72(10):1376-1382.
  11. Danielsson S, Viggedal G, Gillberg C, Olsson I. Lack of effects of vagus nerve stimulation on drug-resistant epilepsy in eight pediatric patients with autism spectrum disorders: a prospective 2-year follow-up study. Epilepsy Behav. 2008; 12(2):298-304.
  12. De Ferrari GM, Crijns HJ, Borggrefe M, et al. Chronic vagus nerve stimulation: a new and promising therapeutic approach for chronic heart failure. Eur Heart J. 2011; 32(7):847-855.
  13. De Herdt V, Boon P, Ceulemans B, et al. Vagus nerve stimulation for refractory epilepsy: a Belgian multicenter study. Eur J Paediatr Neurol. 2007; 11(5):261-269.
  14. Elliott RE, Morsi A, Geller EB, et al. Impact of failed intracranial epilepsy surgery on the effectiveness of subsequent vagus nerve stimulation. Neurosurgery. 2011a; 69(6):1210-1217.
  15. Elliott RE, Morsi A, Kalhorn SP, et al. Vagus nerve stimulation in 436 consecutive patients with treatment-resistant epilepsy: long-term outcomes and predictors of response. Epilepsy Behav. 2011b; 20(1):57-63.
  16. Elliott, RE, Rodgers, SD, Bassani, L, et al. Vagus nerve stimulation for children with treatment-resistant epilepsy: a consecutive series of 141 cases. J Neurosurg Pediatr. 2011c; 7(5):491-450.
  17. Englot DJ, Chang EF, Auguste KI. Vagus nerve stimulation for epilepsy: a meta-analysis of efficacy and predictors of response. J Neurosurg. 2011; 115(6):1248-1255.
  18. Fitzgerald PB, Daskalakis ZJ. The use of repetitive transcranial magnetic stimulation and vagal nerve stimulation in the treatment of depression. Curr Opin Psychiatry. 2008; 21(1):25-29.
  19. George MS, Nahas Z, Borckardt JJ, et al. Vagus nerve stimulation for the treatment of depression and other neuropsychiatric disorders. Expert Rev Neurotherapeutics. 2007; 7(1):63-74.
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  21. Ghaemi K, Elsharkawy AE, Schulz R, et al. Vagus nerve stimulation: outcome and predictors of seizure freedom in long-term follow-up. Seizure. 2010; 19(5):264-268.
  22. Handforth A, Ondo WG, Tatter S, et al. Vagus nerve stimulation for essential tremor: a pilot efficacy and safety trial. Neurology. 2003; 61(10):1401-1405.
  23. Hauptman PJ, Schwartz PJ, Gold MR, et al. Rationale and study design of the increase of vagal tone in heart failure study: INOVATE-HF. Am Heart J. 2012; 163(6):954-962.
  24. Jaseja H. Vagal nerve stimulation: exploring its efficacy and success for an improved prognosis and quality of life in cerebral palsy patients. Clin Neurol Neurosurg. 2008; 110(8):755-762.
  25. Kabir SM, Rajaraman C, Rittey C, et al. Vagus nerve stimulation in children with intractable epilepsy: indications, complications and outcome. Childs Nerv Syst. 2009; 25(9):1097-1100.
  26. Kostov K, Kostov H, Taubøll E. Long-term vagus nerve stimulation in the treatment of Lennox-Gastaut syndrome. Epilepsy Behav. 2009; 16(2):321-324.
  27. Kostov H, Larsson PG, Roste GK. Is vagus nerve stimulation a treatment option for patients with drug-resistant idiopathic generalized epilepsy? Acta Neurol Scand Suppl. 2007; 187:55-58.
  28. Lange G, Janal MN, Maniker A, et al. Safety and efficacy of vagus nerve stimulation in fibromyalgia: a phase I/II proof of concept trial. Pain Med. 2011; 12(9):1406-1413.
  29. Marangell LB, Rush AJ, George MS, et al. Vagus nerve stimulation (VNS) for major depressive episodes: one-year outcomes. Biol Psychiatry. 2002; 51(4):280-287.
  30. Mathew NT. Dynamic optimization of chronic migraine treatment: current and future options. Neurology. 2009; 72(5 Suppl):S14-20.
  31. Mauskop A. Vagus nerve stimulation relieves chronic refractory migraine and cluster headaches. Cephalgia. 2005; 25(2):82-86.
  32. Merrill CA, Jonsson MAG, Minthon L, et al. Vagus nerve stimulation in patients with Alzheimer's disease: additional follow-up results of a pilot study through one year. J Clin Psychiatry. 2006; 67(1):1171-1178.
  33. Morris GL, Meuller WM. Long term treatment with vagus nerve stimulation in patients with refractory epilepsy. Neurology. 1999; 53(8):1731-1735.
  34. Murphy JV. Left vagal nerve stimulation in children with medically refractory epilepsy. J Pediat. 1999; (5)134:563-566.
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Government Agency, Medical Society, and Other Authoritative Publications:

  1. Blue Cross Blue Shield Association Technology Evaluation Center. Vagus nerve stimulation for the treatment of resistant depression. August, 2006. TEC Bulletin, 2006: 21(7).
  2. Centers for Medicare and Medicaid Services (CMS). National Coverage Determinations. Vagus nerve stimulation. NCD #160.18. Effective May 4, 2007. Available at: http://www.cms.hhs.gov/mcd/viewncd.asp?ncd_id=160.18&ncd_version=2&basket=ncd%3A160%2E18%3A2%3AVagus+Nerve+Stimulation+for+Treatment+of+Seizures. Accessed on April 29, 2013.
  3. Fisher RS, Handforth A. Reassessment: vagus nerve stimulation for epilepsy. A Report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology. 1999; 53:666-669.
  4. Fisher RS, Krauss GL, Ramsay E, et al. Assessment of vagus nerve stimulation for epilepsy: report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology. 1997; 49(1):293-297.
  5. Gaynes BN, Lux L, Lloyd S, et al. Nonpharmacologic interventions for treatment-resistant depression in adults [Internet]. Rockville, MD: Agency for Healthcare Research and Quality. September 2011. Available at: http://www.effectivehealthcare.ahrq.gov/ehc/products/76/792/TRD_CER33_20111110.pdf. Accessed on April 29, 2013.
  6. Gelenberg AJ, Freeman MP, Markowitz JC, et al. Work Group on Major Depressive Disorder. American Psychiatric Association (APA). Practice guideline for the treatment of patients with major depressive disorder. 3rd Edition. Am J Psychiatry. 2010; 167(10S).
  7. Kennedy SH, Milev R, Giacobbe P, et al. Canadian Network for Mood and Anxiety Treatments (CANMAT) clinical guidelines for the management of major depressive disorder in adults: IV. Neurostimation therapies. J Affect Disord. 2009; 117 Suppl 1:S44-53.
  8. National Institute for Clinical Excellence (NICE). VNS for refractory epilepsy in children. March 16, 2004. Available at: http://www.nice.org.uk/Guidance/IPG50/Guidance/pdf/English. Accessed on April 29, 2013.
  9. U.S. Food and Drug Administration (FDA). Summary of Safety and Effectiveness Data. Stimulator, vagus nerve. Available at: http://www.fda.gov/ohrms/dockets/dockets/05m0283/05m-0283-aav0001-03-SSED-vol1.pdf. Accessed on April 29, 2013.
  10. U.S. National Institutes of Health (NIH). Clinical trials: vagus nerve stimulation. Available at: http://www.clinicaltrials.gov. Accessed on April 29, 2013.
Web Sites for Additional Information
  1. American Academy of Neurology (AAN).Available at: http://www.aan.com/. Accessed on April 29, 2013.
  2. American Association of Neurological Surgeons (AANS). Available at: http://www.aans.org/. Accessed on April 29, 2013.
  3. Epilepsy Foundation. Available at: http://www.epilepsyfoundation.org/. Accessed on April 29, 2013.
  4. National Institute of Neurological Disorders and Stroke (NINDS). Disorder index. NINDS information pages. Available at: http://www.ninds.nih.gov/disorders/disorder_index.htm. Accessed on April 29, 2013.
    • Epilepsy. Updated April 8, 2013.
    • Lennox-Gastaut Syndrome. Updated April 8, 2013.
Index

CardioFit
VBLOC® Vagal Blocking Therapy
VNS Therapy

The use of specific product names is illustrative only. It is not intended to be a recommendation of one product over another, and is not intended to represent a complete listing of all products available.

Document History
StatusDateAction
 01/01/2014Updated Coding section with 01/01/2014 HCPCS changes.
Revised08/08/2013Medical Policy & Technology Assessment Committee (MPTAC) review. Added treatment of heart failure to the VNS investigational and not medically necessary indications and clarified electronic analysis statement. Updated Rationale, Background, Definitions, Coding, References, Web Sites for Additional Information, and Index sections.
 01/01/2013Updated Coding section with 01/01/2013 CPT changes.
Reviewed08/09/2012MPTAC review.
Reviewed08/03/2012Behavioral Health Subcommittee review. Updated Rationale, Background, References, and Web Sites for Additional Information.
Reviewed11/17/2011MPTAC review. Updated Rationale, References, and Web Sites for Additional Information.
Revised11/18/2010MPTAC review. Clarified statement for electronic analysis of an implanted VNS device, that it is medically necessary for monitoring of an appropriately implanted device. Updated the Rationale, Background, Definitions, References, Web Sites for Additional Information and Index.  Updated Coding section to include 01/01/2011 CPT changes; removed 64573 deleted 12/31/2010.
Revised11/19/2009MPTAC review. Added medically necessary statement addressing analysis of an implanted neurostimulator pulse generator system for VNS when criteria are met. Clarified and expanded investigational and not medically necessary statements:  added specific medical conditions and separate statement to address when analysis of an implanted neurostimulator pulse generator system for VNS is investigational and not medically necessary. Updated Description, Rationale, Background, and References. Updated Coding section with 01/01/2010 HCPCS changes.
Reviewed11/20/2008MPTAC review. Rationale, Definitions, and References updated.
 10/01/2008Updated Coding section with 10/01/2008 ICD-9 changes.
Reviewed11/29/2007MPTAC review. Clarified Position Statement. Rationale, Background, Coding and References updated. The phrase "investigational/not medically necessary" was clarified to read "investigational and not medically necessary."
Reviewed12/07/2006MPTAC review. Background/Overview updated. 
Reviewed09/14/2006MPTAC review. References updated. Coding update: removed HCPCS E0752, E0754, E0756 deleted 12/31/05.
 01/01/2006Updated Coding section with 01/01/2006 CPT/HCPCS changes
Revised12/01/2005MPTAC review.
 11/22/2005Added reference for Centers for Medicare and Medicaid Services (CMS) National Coverage Determination (NCD).
Revised09/22/2005MPTAC review.
Revised07/14/2005MPTAC review. Revision based on Pre-merger Anthem and Pre-merger WellPoint Harmonization.
Pre-Merger OrganizationsLast Review DateDocument NumberTitle 
Anthem, Inc.01/28/2004SURG.00007Vagus Nerve Stimulation Therapy
WellPoint Health Networks, Inc.04/28/20052.10.05Vagus Nerve Stimulation