Notification



Notification Issue Date:



Medical Policy Bulletin


Title:Vagus Nerve Stimulation (VNS)

Policy #:11.15.16n

This policy is applicable to the Company’s commercial products only. Policies that are applicable to the Company’s Medicare Advantage products are accessible via a separate Medicare Advantage policy database.


The Company makes decisions on coverage based on Policy Bulletins, benefit plan documents, and the member’s medical history and condition. Benefits may vary based on contract, and individual member benefits must be verified. The Company determines medical necessity only if the benefit exists and no contract exclusions are applicable.

When services can be administered in various settings, the Company reserves the right to reimburse only those services that are furnished in the most appropriate and cost-effective setting that is appropriate to the member’s medical needs and condition. This decision is based on the member’s current medical condition and any required monitoring or additional services that may coincide with the delivery of this service.

This Medical Policy Bulletin document describes the status of medical technology at the time the document was developed. Since that time, new technology may have emerged or new medical literature may have been published. This Medical Policy Bulletin will be reviewed regularly and be updated as scientific and medical literature becomes available. For more information on how Medical Policy Bulletins are developed, go to the About This Site section of this Medical Policy Web site.



Policy

Coverage is subject to the terms, conditions, and limitations of the member's contract.

MEDICALLY NECESSARY

Implantable vagus nerve stimulation (VNS) is considered medically necessary and, therefore, covered for the treatment of individuals who have medically refractory seizures and for whom surgery is not recommended or has failed.

EXPERIMENTAL/INVESTIGATIONAL

IMPLANTABLE VAGUS NERVE STIMULATION
Implantable vagus nerve stimulation is considered experimental/investigational and, therefore, not covered because the safety and/or effectiveness of this service cannot be established by review of the available published peer-reviewed literature in the treatment for conditions, including, but not limited to the following:
  • Chronic heart failure
  • Fibromyalgia
  • Essential tremor
  • Headache/migraine
  • Tinnitus
  • Traumatic brain injury
  • Obesity
    • Although the US Food and Drug Administration (FDA) has approved a device for implantable vagus nerve stimulation for use in the treatment of individuals who have obesity, the Company has determined that the safety and/or effectiveness of this service cannot be established by review of the available published peer-reviewed literature.

NON-IMPLANTABLE VAGUS NERVE STIMULATION
Non-implantable vagus nerve stimulation is considered experimental/investigational and, therefore, not covered because the safety and/or effectiveness of this service cannot be established by review of the available published peer-reviewed literature in the treatment for conditions, including, but not limited to the following:
  • Epilepsy
  • Migraine headaches
    • Although the US Food and Drug Administration (FDA) has approved a device, (i.e. gammaCore™ [non-invasive vagus nerve stimulator (nVNS)]), for non-implantable vagus nerve stimulation for use in the treatment of pain associated with migraine headaches in adults, the Company has determined that the safety and/or effectiveness of this service cannot be established by review of the available published peer-reviewed literature.
  • Cluster headaches
    • Although the US Food and Drug Administration (FDA) has approved a device, (i.e. gammaCore™ [non-invasive vagus nerve stimulator (nVNS)]), for non-implantable vagus nerve stimulation for use in the treatment of pain associated with cluster headaches in adults (including episodic cluster headaches in adults, and as a therapy for adjunctive use for the preventive treatment of cluster headache in adults), the Company has determined that the safety and/or effectiveness of this service cannot be established by review of the available published peer-reviewed literature.

NOT MEDICALLY NECESSARY

Although the US Food and Drug Administration (FDA) has approved devices for implantable vagus nerve stimulation for use in the treatment of individuals who have refractory depression, the Company has determined that the available published peer-reviewed literature does not support the procedure as a useful aid in the treatment of refractory depression. Therefore, implantable vagus nerve stimulation in the treatment of individuals who have refractory depression is considered not medically necessary by the Company and not covered.

REQUIRED DOCUMENTATION

The individual's medical record must reflect the medical necessity for the care provided. These medical records may include, but are not limited to: records from the professional provider's office, hospital, nursing home, home health agencies, therapies, and test reports.

The Company may conduct reviews and audits of services to our members, regardless of the participation status of the provider. All documentation is to be available to the Company upon request. Failure to produce the requested information may result in a denial for the service.
Guidelines

BENEFIT APPLICATION

Subject to the terms and conditions of the applicable benefit contract, vagus nerve stimulation (VNS) is covered under the medical benefits of the Company’s products when the medical necessity criteria listed in this medical policy are met.

US FOOD AND DRUG ADMINISTRATION (FDA) STATUS

On July 16, 1997, the FDA approved the use of the NeuroCybernetic Prosthesis (NCP®) System (Cyberonics, Inc., Houston, TX), a VNS device, for the treatment of partial seizures in adults and children 12 years of age or older. FDA labeling for the treatment of medically refractory partial-onset seizures has not changed to include children younger than 12 years of age. However, the National Institute for Clinical Excellence (NICE) supports the use of VNS for medically refractory epilepsy in children.

On July 15, 2005, the FDA approved the use of the VNS Therapy System NeuroCybernetic Prosthesis (NCP®) System (Cyberonics, Inc., Houston, TX) for the long-term treatment of chronic or recurrent depression in individuals 18 years of age or older who have experienced a major depressive episode and have not adequately responded to four or more antidepressant treatments.

On January 14, 2015, the FDA approved the MAESTRO® Rechargeable System (EnteroMedics, St. Paul, MN), for use in weight reduction in individuals aged 18 years through adulthood who have a Body Mass Index (BMI) of 40 to 45 kg/m2, or a BMI of 35 to 39.9 kg/m2 with one or more obesity related co-morbid conditions, and have failed at least one supervised weight management program within the past five years.

FDA has approved the gammaCore® Non-invasive Vagus Nerve Stimulator (electroCore, Basking Ridge, NJ)for:
  • use in acute treatment of pain associated with episodic cluster headache in adult patients subject to the special controls identified
  • use in acute treatment of pain associated with episodic migraine headache in adult patients
  • adjunctive use for the preventive treatment of cluster headache in adult patients.


Description

VAGUS NERVE STIMULATION AS A TREATMENT OF MEDICALLY AND SURGICALLY REFRACTORY SEIZURES

Vagus nerve stimulation (VNS) has been evaluated as an alternative treatment for individuals with medically refractory seizures for whom surgery is not recommended or has failed. Seizures that are not completely controlled by medical therapy, or seizures that cannot be treated with therapeutic levels of antiepileptic drugs because of intolerable adverse effects of these drugs, are referred to as medically refractory seizures.

Seizures are considered paroxysmal disorders (i.e., characterized by abnormal cerebral neuronal discharge) and occur when there is errant electrical discharge activity in the brain. Seizures cause different physical symptoms depending on the location of the electrical activity in the brain. They may be mild to severe, ranging from causing a slight tingling sensation or momentary confusion to causing complete unconsciousness. Classification and subtypes of seizures are commonly diagnosed by electroencephalography (EEG). Seizures are classified as simple partial, complex partial, and generalized onset, and are distinguished on the basis of the level of consciousness.

Partial seizures affect only a portion, or one hemisphere, of the brain and are subdivided into the following:
  • Simple partial seizures
    • Awareness is unimpaired; there is no alteration of consciousness.
  • Complex partial seizures
    • Awareness is impaired; an alteration of consciousness is usually involved.
  • Simple or complex partial seizures that may become secondarily generalized, leading to tonic, clonic, or tonic-clonic seizures
    • There is complete loss of consciousness.

Generalized seizures are caused by errant electrical activity in multiple locations, or large areas, that may involve both the left and the right hemispheres of the brain. This type of seizure has a more complex set of symptoms, with impaired awareness leading to complete loss of consciousness. The subtypes of generalized seizures are usually classed as follows:
  • Absence seizures (formerly petit mal)
    • Awareness is briefly impaired, sometimes accompanied by mild clonic, tonic, or atonic components. Onset and endings are abrupt.
  • Atypical absence seizures
    • More marked symptoms, and more gradual onset and ending than occur in typical absence seizures.
  • Myoclonic seizures
    • Awareness is usually not impaired, with single or multiple sudden contractions of muscle groups.
  • Tonic-clonic seizures (formerly grand mal)
    • Usually complete loss of consciousness accompanied by sudden, brief muscle contractions.

Epilepsy is diagnosed in individuals who have a predisposition for recurrent, unprovoked seizures. During the past 10 years, new medications and surgical techniques have emerged in the treatment of epilepsy. Despite these advances, 20 percent to 50 percent of individuals with epilepsy have breakthrough seizures or experience adverse effects of anti-seizure medications. Current peer-reviewed medical literature supports VNS as a useful palliative procedure for individuals who have severe generalized epilepsy with atonic or tonic-clonic seizures. Peer-reviewed literature also supports the use of VNS as an effective treatment for medically refractory seizures other than partial-onset seizures.

The VNS system is composed of an implantable generator, a bipolar electrical lead (array) consisting of helical electrodes and an anchor tether, along with an external programming device that is used to change stimulation settings. Revisions to the VNS system may include procedures such as replacing the battery-powered generator. Battery longevity depends on stimulation parameters, with newer battery-powered generators lasting up to 10 years or more. The generator is surgically implanted subcutaneously, at the lateral border of the left pectoral muscle, or under the arm. An incision is also made to the left side of the neck, to access the vagus nerve, for the placement of the electrodes. The lead (array) is threaded subcutaneously to connect the electrodes, which are attached to the vagus nerve, to the generator. Once implantation is completed, the generator is programmed to stimulate the vagus nerve at regular intervals.

The basic principles of VNS when used as a treatment for epilepsy are that vagal visceral afferents (nerves that convey impulses from sense organs and other receptors to the brain or spinal cord) have a diffuse central nervous system projection, and the activation of these pathways has a widespread effect upon neuronal excitability. The exact mechanism of VNS on neuronal excitability is not fully known. Adverse effects of VNS therapy include headache, neck pain, cough, and voice alterations.

Some of the benefits of using VNS may include less-severe or shorter seizures, a reduction in seizure frequency, improved recovery periods after seizures, and a lessening of seizure clusters. Individuals undergoing VNS must be aware that seizure control improves over time, and that although VNS may reduce the frequency and magnitude of seizure activity, the need remains for an ongoing, concurrent, anti-seizure medicinal regimen.

On July 16, 1997, the US Food and Drug Administration (FDA) approved the NeuroCybernetic Prosthesis (NCP®) System (Cyberonics, Inc., Houston, TX), a VNS device, for the treatment of partial seizures in adults and children 12 years of age or older. Studies since the original FDA approval have focused on the use of VNS in younger children. FDA labeling for the treatment of medically refractory partial-onset seizures has not changed to include children younger than 12 years of age. Currently, VNS for children younger than 12 years of age is considered an off-label use of the device. The National Institute for Health and Clinical Excellence (NICE) guidelines support the use of VNS for refractory epilepsy in children only if all of the following criteria are met:
  • The procedure is performed by a specialized pediatric epilepsy team.
  • The procedure is directed by developmentally appropriate pre- and post-device implantation.
  • There is post-procedure quality-of-life monitoring.

VAGUS NERVE STIMULATION AS A TREATMENT OF REFRACTORY DEPRESSION

On July 15, 2005, the FDA approved the VNS Therapy System, NeuroCybernetic Prosthesis (NCP®) System (Cyberonics, Inc., Houston, TX) for use as an adjunctive treatment for chronic or recurrent depression in individuals 18 years of age or older who have experienced a major depressive episode and have not adequately responded to four or more antidepressant treatments. Despite FDA approval, current published peer-reviewed literature does not support the use of VNS for the treatment of depression. The clinical trials for the use of VNS for treatment-resistant depression (TRD) do not demonstrate the effectiveness of VNS therapy on health outcomes in an investigational setting, nor do these trials demonstrate improved health outcomes with the use of VNS when compared to other treatment modalities for TRD. Additional research is recommended.

VAGUS NERVE STIMULATION AS A TREATMENT OF OTHER CONDITIONS

VNS therapy has also been investigated for use in other conditions; however, the available published peer-reviewed evidence is limited and not sufficient to permit conclusions of effectiveness.

In a study examining the safety and efficacy of VNS in individuals with chronic heart failure, De Ferrari et al (2011) showed improvements in New York Heart Association (NYHA) class quality of life, six-minute walk test, and left ventricular ejection fraction; however, these findings require confirmation in controlled clinical trials. A multicenter, randomized clinical trial called INOVATE-HF (INcrease Of VAgal TonE in chronic Heart Failure) investigating the safety and efficacy of an implantable vagus nerve electrical stimulation device called CardioFit® for the treatment of individuals with heart failure showed VNS does not reduce the rate of death or heart failure events in chronic heart failure individuals.

VNS has been investigated for use in fibromyalgia. Lange et al (2011) conducted a single-arm Phase I/II trial of 14 individuals with fibromyalgia. At three months, five individuals met criteria for improvement of symptoms, at 11 months, eight individuals met efficacy criteria. However, the results do not provide sufficient evidence for use of VNS for fibromyalgia.

Handforth et al (2003) studied VNS in nine individuals with essential tremor resulting in no improvement in upper extremity tremors. The authors of the study reported that VNS is not likely to have any clinically meaningful effect in essential tremor treatment.

Bodenlos et al (2007) suggested that VNS might affect food cravings of individuals with chronic, treatment-resistant depression and thus induce weight loss in obese individuals. Several limitations in the study such as small sample size, lack of randomization, heterogeneity of groups with respect to depression, prevent drawing conclusions about the impact of VNS on eating behavior. The study findings need to be validated in large, well-designed controlled studies to evaluate the impact of VNS on eating behavior and obesity.

On January 14, 2015, the FDA approved the MAESTRO® Rechargeable System (EnteroMedics, St. Paul, MN), consisting of a rechargeable neuroregulator device implanted into the lateral chest wall with flexible leads placed laparoscopically around the vagus nerve, for use in weight reduction in individuals aged 18 years through adulthood who have a Body Mass Index (BMI) of 40 to 45 kg/m2, or a BMI of 35 to 39.9 kg/m2 with one or more obesity-related co-morbid conditions, and have failed at least one supervised weight management program within the past five years. The approval is based on a 12-month randomized, double-blind, sham controlled clinical trial involving 239 participants. Despite FDA approval, several limitations in this study include the use of vagal nerve block compared with a sham control device did not meet either of the pre-specified co-primary efficacy objectives. The co-primary effectiveness endpoints were to determine whether the vagal nerve block was superior in mean percentage excess weight loss to sham by a 10-point margin with at least 55 percent of individuals in the vagal block group achieving a 20 percent loss and 45 percent achieving a 25 percent loss, even though weight loss in the vagal block group was greater than in the sham device group. In addition, the treatment arm participants could possibly feel the stimulation device, while the control arm doesn’t feel anything, so individuals may lose motivation to participate and not adhere to diet program, which would limit their weight loss, causing weight loss in the vagal block group to be greater than in the sham device group. Because the study did not compare outcomes with established surgical obesity treatments (e.g., gastric banding, Roux-en Y gastric bypass), because of the short-term follow-up period without long-term outcomes of vagal nerve stimulation for morbid obesity, at this time there is inadequate data to permit scientific conclusions regarding the efficacy of this procedure.

Vagal nerve stimulation is being studied for treating chronic headaches. Mauskop (2005) evaluated VNS in five individuals with severe, refractory chronic cluster and migraine headaches. One individual had excellent results with regaining the ability to work, and two individuals reported significant improvement of their headaches. Small sample size prevents drawing conclusions on the effects of VNS for the treatment of headache.

The clinical efficacy of VNS on tinnitus was studied by De Ridder et al (2013) in a case series involving 10 individuals that suggests that VNS may be associated with clinical improvements in individuals with tinnitus. The findings of this study need to be validated in large, well-designed controlled studies to evaluate the impact of VNS on tinnitus.

Currently, VNS is being investigated to augment recovery from a traumatic brain injury. It is proposed that early stimulation of the vagus nerve accelerates the rate and extent of behavioral and cognitive recovery after fluid percussion brain injury in rats. Shi et al (2013) received FDA approval to conduct a pilot prospective randomized trial to demonstrate objective improvement in clinical outcome by placement of a VNS in individuals who are recovering from severe traumatic brain injury. If this study demonstrates that VNS can safely and positively impact outcome, then a larger randomized prospective crossover trial will be proposed.

NON-IMPLANTABLE TRANSCUTANEOUS VAGUS NERVE STIMULATION

Transcutaneous vagus nerve stimulation (tVNS) is being investigated as a noninvasive alternative to surgery for numerous indications. For example, the transcutaneous VNS (t-VNS®) system uses a non-invasive approach that combines a stimulation unit and ear electrode to stimulate the auricular branch of the vagus nerve (which supplies the skin over the concha of the ear) for the treatment of pharmacoresistant epilepsy. Individuals self-administer electric stimulation for several hours per day. Currently, the device does not have FDA approval.

National Institute for Health and Care Excellence (NICE) interventional procedures guidance on “Transcutaneous stimulation of the cervical branch of the vagus nerve for cluster headache and migraine” (2016) stated that “Current evidence on the safety of transcutaneous stimulation of the cervical branch of the vagus nerve for cluster headache and migraine raises no major concerns.  The evidence on efficacy is limited in quantity and quality.  Therefore, this procedure should only be used with special arrangements for clinical governance, consent and audit or research … Clinicians wishing to do transcutaneous stimulation of the cervical branch of the vagus nerve for cluster headache and migraine should ensure that patients understand the uncertainty about the procedure's efficacy and provide them with clear written information … NICE encourages further research on transcutaneous stimulation of the cervical branch of the vagus nerve for cluster headache and migraine.  Studies should describe whether the procedure is used for treatment or prevention, and whether it is used for cluster headache or migraine.  Clinicians should clearly document details of patient selection and the treatment regimen.  Outcome measures should include changes in the number and severity of cluster headache or migraine episodes, medication use, quality of life in the short and long term, side effects, acceptability, and device durability”.

GAMMACORE® NON-INVASIVE VEGAS NERVE STIMULATOR (BY ELECTROCORE) FOR THE PROPHYLAXIS AND TREATMENT OF CLUSTER AND MIGRAINE HEADACHES

In an open-label, single-arm, pilot study, Goadsby et al (2014) evaluated a novel, non-invasive, portable vagal nerve stimulator (nVNS) for acute treatment of migraine.  Participants with migraine (with or without aura) were eligible for this study.  Up to 4 migraine attacks were treated with two 90-second doses, at 15-minute intervals delivered to the right cervical branch of the vagus nerve within a 6-week time period.  Subjects were asked to self-treat at moderate or severe pain, or after 20 minutes of mild pain.  Of 30 enrolled patients (25 females, 5 males, median age of 39 years), 2 treated no attacks, and 1 treated aura only, leaving a full analysis set of 27 treating 80 attacks with pain.  An adverse event was reported in 13 patients, notably: neck twitching (n = 1), raspy voice (n = 1) and redness at the device site (n = 1).  No un-anticipated, serious or severe adverse events were reported.  The pain-free rate at 2 hours was 4 of 19 (21 %) for the first treated attack with a moderate or severe headache at baseline.  For all moderate or severe attacks at baseline, the pain-free rate was 12/54 (22 %).  The authors concluded that nVNS may be an effective and well-tolerated acute treatment for migraine in certain patients.  These preliminary findings need to be validated by well-designed studies.

Nesbitt et al (2015) reported their initial experience with a novel device, designed to provide portable, non-invasive, transcutaneous stimulation of the vagus nerve, both acutely and preventively, as a treatment for cluster headache.  Patients with cluster headache (11 chronic, 8 episodic), from 2 centers, including 7 who were refractory to drug treatment, had sufficient data available for analysis in this open-label observational cohort study.  The device, known as the gammaCore, was used acutely to treat individual attacks as well as to provide prevention.  Patient-estimated efficacy data were collected by systematic inquiry during follow-up appointments up to a period of 52 weeks of continuous use.  A total of 15 patients reported an overall improvement in their condition, with 4 reporting no change, providing a mean overall estimated improvement of 48 %.  Of all attacks treated, 47 % were aborted within an average of 11 ± 1 minutes of commencing stimulation; 10 patients reduced their acute use of high-flow oxygen by 55 % with 9 reducing use of triptan by 48 %.  Prophylactic use of the device resulted in a substantial reduction in estimated mean attack frequency from 4.5/24 hours to 2.6/24 hours (p < 0.0005) post-treatment.  The authors concluded that these data suggested that non-invasive vagus nerve stimulation may be practical and effective as an acute and preventive treatment in chronic cluster headaches.  They stated that further evaluation of this treatment using randomized sham-controlled trials is thus warranted.  This study provided Class IV evidence that for patients with cluster headache, transcutaneous stimulation of the vagus nerve aborts acute attacks and reduces the frequency of attacks.

Puledda and Goadsby (2016) stated that neuromodulation is a promising, novel approach for the treatment of primary headache disorders.  Neuromodulation offers a new dimension in the treatment that is both easily reversible and tends to be very well-tolerated.  The autonomic nervous system is a logical target given the neurobiology of common primary headache disorders, such as migraine and the trigeminal autonomic cephalalgias (TACs).  These investigators reviewed new encouraging results of studies from the most recent literature on neuromodulation as acute and preventive treatment in primary headache disorders, and discussed some possible underlying mechanisms.  These researchers focused on vagal nerve stimulation (VNS) and spheno-palatine ganglion stimulation (SPGS) since they have targeted autonomic pathways that are cranial and can modulate relevant pathophysiological mechanisms.  The initial data suggested that these approaches will find an important role in headache disorder management going forward.  The authors concluded that the armamentarium for the treatment of migraine and the TACs is rapidly expanding thanks to neuromodulation techniques.  The newer methods appear much better tolerated and offer important therapeutic benefits.  Equally attractive in many ways is that bench-based understanding is being applied to neuromodulation to yield bedside advances in treatment.  They stated that clinicians can look forward to the results of a number of ongoing studies and the real possibility to add these exciting methods to their practice.

In a randomized, double-blind, sham-controlled study, Silberstein and colleagues (2016) evaluated nVNS as an acute CH treatment.  A total of 150 subjects were enrolled and randomized (1:1) to receive nVNS or sham treatment for less than or equal to 1 month during a double-blind phase; completers could enter a 3-month nVNS open-label phase.  The primary end-point was response rate, defined as the proportion of subjects who achieved pain relief (pain intensity of 0 or 1) at 15 minutes after treatment initiation for the first CH attack without rescue medication use through 60 minutes; secondary end-points included the sustained response rate (15 to 60 minutes).  Sub-analyses of episodic cluster headache (eCH) and chronic cluster headache (cCH) cohorts were pre-specified.  The intent-to-treat population comprised 133 subjects: 60 nVNS-treated (eCH, n = 38; cCH, n = 22) and 73 sham-treated (eCH, n = 47; cCH, n = 26).  A response was achieved in 26.7 % of nVNS-treated subjects and 15.1 % of sham-treated subjects (p = 0.1).  Response rates were significantly higher with nVNS than with sham for the eCH cohort (nVNS, 34.2 %; sham, 10.6 %; p = 0.008) but not the cCH cohort (nVNS, 13.6 %; sham, 23.1 %; p = 0.48).  Sustained response rates were significantly higher with nVNS for the eCH cohort (p = 0.008) and total population (p = 0.04).  Adverse device effects (ADEs) were reported by 35/150 (nVNS, 11; sham, 24) subjects in the double-blind phase and 18/128 subjects in the open-label phase.  No serious ADEs occurred.  The authors concluded that in one of the largest randomized sham-controlled studies for acute CH treatment, the response rate was not significantly different (versus sham) for the total population; nVNS provided significant, clinically meaningful, rapid, and sustained benefits for eCH but not for cCH, which affected results in the total population.  They stated that this safe and well-tolerated treatment represents a novel and promising option for eCH.

The authors noted that the drawbacks of this study included the analysis of the cCH cohort as part of the primary end-point, the need for careful interpretation of sub-analyses results, challenges with blinding inherent in medical device studies, and the time to first measurement of response used to define the primary efficacy end-point.  Primary end-point results were significant for the eCH cohort but were diminished overall by the cCH cohort results.  When sub-analyses results were interpreted, the lack of statistical powering and the potential for type 1 and type 2 errors (in the eCH and cCH cohorts, respectively) should be considered.  The difference in AE descriptions provided by subjects treated with the nVNS (e.g., drooping/pulling of the lip/face) and sham (e.g., burning, soreness, stinging) devices may help to explain results of the blinding analyses, which were similar to those observed in previous sham-controlled trials.  The burning sensation and other pain-related AEs reported by the sham-treated group in ACT1 may have led to a placebo effect based on impressions that the subjects were receiving active treatment.  Sham device-associated pain may have also produced a diffuse noxious inhibitory control (DNIC) effect, a phenomenon in which the application of a noxious electrical stimulus to remote body regions inhibits dorsal horn activity and attenuates the original pain.  Potential placebo and DNIC effects in the sham group may have reduced the magnitude of the therapeutic benefit associated with nVNS treatment.  Another drawback was that the time-point used to define the ACT1 primary end-point was 15 minutes after treatment initiation, which has been used in other CH studies, rather than after treatment completion.  In ACT1, this 15-minute interval comprised an 8‐minute nVNS stimulation period followed by only a 7-minute period that appeared to be sufficient for significant treatment effects to become evident in the eCH cohort but not in the cCH cohort or total population.  The 15-minute assessment time-point may have also contributed to the non-significant difference in average pain intensities between the nVNS and sham groups; other potential contributing factors include the combined statistical influence of the responders and non-responders as well as the assessment after all attacks (rather than after the first attack).  Thus, methodological implications in ACT1 regarding distinct effects among the eCH and cCH cohorts, the painful sham stimulation, and the use of a longer time-point to first measurement of response such as 30 minutes, as used in CH studies of other therapies, should be considered for future RCTs.

In a prospective, open-label, randomized study, Gaul and associates (2016) compared adjunctive prophylactic nVNS (n = 48) with standard of care (SoC) alone (control; n = 49) for the acute treatment of cCH.  A 2-week baseline phase was followed by a 4-week randomized phase (SoC plus nVNS versus control) and a 4-week extension phase (SoC plus nVNS).  The primary end-point was the reduction in the mean number of CH attacks per week.  Response rate, abortive medication use and safety/tolerability were also assessed.  During the randomized phase, individuals in the intent-to-treat population treated with SoC plus nVNS (n = 45) had a significantly greater reduction in the number of attacks per week versus controls (n = 48) (-5.9 versus -2.1, respectively) for a mean therapeutic gain of 3.9 fewer attacks per week (95 % CI: 0.5 to 7.2; p = 0.02).  Higher (greater than or equal to 50 %) response rates were also observed with SoC plus nVNS (40 % (18/45)) versus controls (8.3 % (4/48); p < 0.001).  No serious treatment-related adverse events occurred.  The authors concluded that adjunctive prophylactic nVNS is a well-tolerated novel treatment for chronic CH, offering clinical benefits beyond those with SoC.

The authors stated that study limitations included the lack of a placebo/sham device, an open-label study design, the short treatment duration and the use of patient-reported outcomes.  No placebo arm was incorporated into the study because a suitable placebo/sham device had not yet been designed.  Instead of a placebo/sham arm, SoC was deemed the most appropriate control treatment that was reflective of a real-world clinical scenario.  The open-label study design and short treatment duration may have contributed to a placebo effect in both treatment groups.  The 16.7 % response rate in the control group during the extension phase may partially reflect a placebo response to nVNS.  The initial response experienced in the control group during the randomized phase may have also impacted the capacity for a meaningful response to nVNS during the extension phase.  Furthermore, fewer individuals in the control arm (50 %) than in the nVNS arm (64.4 %) were highly adherent (greater than or equal to 80 %) to prophylactic nVNS, which may have further confounded response rates and reductions in abortive medication use in this group.  Only patients with chronic, treatment-refractory CH were included because of their stable CH attack frequency and intensity.  A 2.5-month study duration was deemed sufficient to observe a treatment effect.  Treatment response in favor of nVNS was consistent across intent-to-treat (ITT), modified ITT (mITT) and per-protocol populations (per-protocol population was defined as participants in the mITT population who had greater than or equal to 12 days of observation in the randomized phase and no major protocol violation).  Because no CH-specific QoL instruments exist, the EQ-5D-3L and HIT-6 measures were considered most appropriate, and nVNS prophylaxis resulted in meaningful improvements for both measures.  The apparent lack of effect of acute nVNS therapy on CH duration or severity was consistent with findings in the chronic CH population that were reported in a recent study of acute nVNS therapy for CH.  The nVNS adherence rates in this study (50  to 64 %) were consistent with those reported for prophylactic non-invasive neuromodulation in migraine and were considered meaningful given that twice-daily nVNS requires more effort and participation than a conventional oral medication regimen.

On April 14, 2017, the FDA approved the gammaCore nVNS for the acute treatment of pain associated with eCH in adult patients.

Yuan and Silberstein (2017) stated that neuromodulation is an emerging area in headache management.  Through neurostimulation, multiple brain areas can be modulated to alleviate pain, hence reducing the pharmacological need.  These investigators discussed the recent development of the VNS for headache management.  Early case series from epilepsy and depression cohorts using invasive VNS showed a serendipitous reduction in headache frequency and/or severity.  Non-invasive VNS, which stimulates the carotid vagus nerve with the use of a personal handheld device, also demonstrated efficacy for acute migraine or CH attacks.  Long-term use of nVNS appeared to exert a prophylactic effect for both chronic migraine and cCH.  In animal studies, nVNS modulated multiple pain pathways and even lessen cortical spreading depression.  Progression in nVNS clinical efficacy over time suggests an underlying disease-modifying neuromodulation.  The authors concluded that nVNS appears to be as effective as the invasive counterpart for many indications.  They noted that with an enormous potential therapeutic gain and a high safety profile, further development and application of nVNS is promising.

In a recent review, Lainez and Guillamon (2017) summarized CH pathophysiology and the effectiveness of various neuromodulating techniques.  In patients with cCH, VNS with a portable device used in conjunction with SoC in CH patients resulted in a reduction in the number of attacks.  The authors concluded that new recent non-invasive approaches such as nVNS have shown effectiveness in a few trials and could be an interesting alternative in the management of CH, but require more testing and positive RCTs.

Miller and colleagues (2017) noted that there is growing interest in neuromodulation for primary headache conditions.  Invasive modalities such as ONS, deep brain stimulation (DBS) and SPGS are reserved for the most severe and intractable patients.  Non-invasive options such as VNS, SONS and TMS have all emerged as potentially useful headache treatments.  These researchers examined the evidence base for non-invasive neuromodulation in TACs and migraine.  Although a number of open-label series of non-invasive neuromodulation devices have been published, there is very little controlled evidence for their use in any headache condition.  Open-label evidence suggested that VNS may have a role in the prophylactic treatment of CH and there is limited evidence to suggest it may be useful in the acute treatment of cluster and potentially migraine attacks.  There is limited controlled evidence to suggest a role for SONS in the prophylactic treatment of episodic migraine, however, there is no evidence to support its use in CH; TMS may be effective in the acute treatment of episodic migraine; but there is no controlled evidence to support its use as a preventative in any headache condition.  The authors concluded that non-invasive neuromodulation techniques are an attractive treatment option with excellent safety profiles, however, their use is not yet supported by high-quality RCTs.

Furthermore, an UpToDate review on “Cluster headache: Treatment and prognosis” (may, 2017) states that “When chronic cluster headache is unresponsive to medical treatments, various surgical interventions and neurostimulation techniques are potential treatment options, though none are clearly established as effective.  In such cases, it is particularly important to exclude potential causes of secondary cluster headache.  Neurostimulation techniques, including sphenopalatine ganglion stimulation and vagus nerve stimulation, appear promising but remain investigational.  Destructive surgical procedures are unproven and should be viewed with great caution”.

Mwamburi  and colleagues (2017a) noted that CH is a debilitating disease characterized by excruciatingly painful attacks that affects 0.15 % to 0.4 % of the US population.  Episodic cluster headache manifests as circadian and circannual seasonal bouts of attacks, each lasting 15 to 180 minutes, with periods of remission.  In cCH, the attacks occur throughout the year with no periods of remission.  While existing treatments are effective for some patients, many patients continue to suffer.  There are only 2 FDA-approved medications for eCH in the United States, while others, such as high-flow oxygen, are used off-label.  Episodic CH is associated with co-morbidities and affects work, productivity, and daily functioning.  The economic burden of eCH is considerable, costing more than twice that of non-headache patients.  These researchers stated that gammaCore adjunct to SoC was found to have superior efficacy in treatment of acute eCH compared with sham-gammaCore used with SoC in ACT1 and ACT2 trials.  However, the economic impact has not been characterized for this indication.  These investigators conducted a cost-effectiveness analysis of gammaCore adjunct to SoC compared with SoC alone for the treatment of acute pain associated with eCH attacks.  The model structure was based on treatment of acute attacks with 3 outcomes: (i) failures, (ii) non-responders, and (iii) responders.  The time horizon of the model is 1 year using a payer perspective with uncertainty incorporated.  Parameter inputs were derived from primary data from the RCTs for gammaCore.  The mean annual costs associated with the gammaCore-plus-SoC arm was $9,510, and mean costs for the SoC-alone arm was $10,040.  The mean quality-adjusted life years for gammaCore-plus-SoC arm were 0.83, and for the SoC-alone arm, they were 0.74.  The gammaCore-plus-SoC arm was dominant over SoC alone.  All 1-way and multi-way sensitivity analyses were cost-effective using a threshold of $20,000.  The authors concluded that gammaCore dominance, representing savings, was driven by superior efficacy, improvement in QOL, and reduction in costs associated with successful and consistent abortion of episodic attacks.  They stated that these findings serve as additional economic evidence to support coverage for gammaCore.  Moreover, they stated that additional real-world data are needed to characterize the long-term impact of gammaCore on co-morbidities, utilization, QOL, daily functioning, productivity, and social engagement of these patients, and for other indications.

Mwamburi  and colleagues (2017b) stated that the FDA has cleared gammaCore (nVNS) for the treatment of eCH.  With the exception of subcutaneous sumatriptan, all other treatments are used off-label and have many limitations.  The FDA approval process for devices differs from that of drugs.  These researchers performed a review of the literature to evaluate new evidence on various aspects of gammaCore treatment and impact.  The ACute Treatment of Cluster Headache Studies (ACT1 and ACT2), both double-blind sham-controlled randomized trials, did not meet the primary end-points of the trials; but each demonstrated significant superiority of gammaCore among patients with eCH.  In ACT1, gammaCore resulted in a higher response rate (RR) (RR, 3.2; 95 % CI: 1.6 to 8.2; p = 0.014), higher pain-free rate for greater than 50 % of attacks (RR, 2.3; 95 % CI: 1.1 to 5.2; p = 0.045), and shorter duration of attacks (MD, -30 minutes; p < 0.01) compared with the sham group.  In ACT2, gammaCore resulted in higher odds of achieving pain-free attacks in 15 minutes (OR, 9.8; 95 % CI: 2.2 to 44.1; p = 0.01), lower pain intensity in 15 minutes (MD, -1.1; p < 0.01), and higher rate of achieving responder status at 15 minutes for greater than or equal to 50 % of treated attacks (RR, 2.8; 95 % CI: 1.0 to 8.1; p = 0.058) compared with the sham group.  The PREVention and Acute Treatment of Chronic Cluster Headache (PREVA) study also demonstrated that gammaCore plus SoC was superior to SoC alone in patients with cCH.  Medical costs, pharmacy refills, and pharmacy costs were higher in patients coded for CH in claims data compared with controls with non-headache codes.  These researchers stated that gammaCore is easy to use, practical, and safe; delivery cannot be wasted; and patients prefer using gammaCore compared with SoC.  The treatment improved symptoms and reduces the need for CH rescue medications.  They stated that current US reimbursement policies, which predated nVNS and are based on expensive, surgically implanted, and permanent implanted vagus nerve stimulation (iVNS), need to be modified to distinguish nVNS from iVNS.  The authors concluded that there is sufficient evidence to support the need to modify current reimbursement policies to include coverage for gammaCore (nVNS) for eCH.  Moreover, they stated that 1 drawback was that the information available from publications that contribute to a review was as reported.  This review, however, added new information to the body of evidence, particularly in comparison with previous reviews.  While authors of previous reviews had identified gammaCore as a beneficial intervention for patients with CH, they also pointed to a gap and a need for clinical trials to provide further evidence on its safety and effectiveness.  They stated that the recommended future path is to collect real-world data that are specific to patients suffering from eCH and CH with regard to use or non-use of gammaCore via a registry to monitor usage and performance measurement.  Additionally, stakeholders should periodically review data from claims databases to evaluate long-term outcomes related to symptoms, utilization, cost, and reimbursement burden and the impact on co-morbidities and all-cause healthcare utilization, to better understand the value associated with gammaCore use beyond symptom relief.  Also needed are continued research efforts, using RCTs, to characterize the benefits of gammaCore in other indications, including migraine, specific inflammatory illnesses, cardiac diseases, and psychiatric disorders.

Silberstein and colleagues (2017) noted that a panel of 9 experts, including neurologists, other headache specialists, and medical and pharmacy directors, from 4 health plans (1 integrated delivery network and 3 plans with commercial, Medicare, and Medicaid lines of business), convened to discuss CH.  Topics covered included the current treatment landscape, treatment challenges, economic impact of disease, and gaps in care for patients with CH.  One major challenge in the management of CH is that it is under-recognized and frequently misdiagnosed, leading to delays in and suboptimal treatment for patients who suffer from this painful and disabling condition.  The management of CH is challenging due to the lack of a robust evidence base for preventive treatment, the AEs associated with conventional preventive treatments, the variability of response to acute treatments, and the challenging reimbursement landscape for well-accepted treatments (e.g., oxygen).  The lack of effective prevention for many patients may lead to the excessive use of acute therapies, often multiple times each day, which drives the cost of illness up significantly.  The goal of the panel discussion was to discuss the role of gammaCore, the recently released first nVNS therapy in the acute treatment of patients with eCH, in the management of CH.  The panel reviewed current practices and formulated recommendations on incorporating a newly released therapy into CH management. The panel explored the role of traditional management strategies as well as that of gammaCore in the acute treatment of patients with eCH.  The panel agreed that the treatment guidelines should be updated to reflect the role of gammaCore as a first-line, acute therapeutic option for patients with eCH and that payers should offer coverage of gammaCore to their members who have a diagnosis of eCH.  Healthcare providers, including headache specialists and neurologists, and payers are encouraged to remain up-to-date regarding the results of ongoing clinical trials evaluating the use of gammaCore for the acute and/or preventive treatment of migraine to ensure that patients are being appropriately treated for these conditions and that they have access to treatment through their insurers.  Moreover, the panel noted that additional studies need to be conducted in the United States to verify the role of gammaCore in the preventive therapy of eCH and cCH.

Simon and Blake (2017) noted that stimulation of the cervical vagus nerve with iVNS has been used clinically for more than 20 years to treat patients with epilepsy.  More recently, gammaCore, a nVNS, was developed, which has been purported to also stimulate the vagus nerve without the cost and morbidity associated with an iVNS system.  gammaCore has been used to acutely treat various types of primary headaches, including migraine and CH, and for the prevention of episodic, chronic, and menstrual migraines and CH.  The gammaCore device was cleared by the FDA for the acute treatment of pain in eCH patients.  These investigators summarized the clinical work that has been published in the use of gammaCore for treating primary headache disorders, presented an overview of studies demonstrating that nVNS does indeed stimulate similar vagus nerve fibers as the implantable VNS system, and then presented several animal headache-related studies that address the mechanism of action (MOA) of nVNS.  The authors concluded that preliminary clinical studies in various primary headache disorders are encouraging.  Human studies and modeling have demonstrated that nVNS activates vagus nerve fibers similar to those implicated in the clinical benefits of iVNS.  They stated that continuing human and animal research is needed to further elucidate the MOA and to help define optimal signal parameters and treatment paradigms for headache and other disorders.

Gaul and associates (2017) stated that although the PREVA trial did not examine the effects of nVNS in patients with eCH, the rapid beneficial effects on attack frequency observed within 2 weeks of treatment initiation in this cCH analysis, combined with the established safety profile of nVNS, suggested that a trial in eCH would be clinically reasonable.

Ho and co-workers (2017) noted that SPG is the largest collection of neurons in the calvarium outside of the brain.  Over the past century, it has been a target for interventional treatment of head and facial pain due to its ease of access.  Block, radiofrequency ablation (RFA), and neuro-stimulation have all been applied to treat a myriad of painful syndromes.  Despite the routine use of these interventions, the literature supporting their use has not been systematically summarized.  These investigators summarized the level of evidence supporting the use of SPG block, RFA and neuro-stimulation.  Medline, Google Scholar, and the Cochrane Central Register of Controlled Trials (CENTRAL) databases were reviewed for studies on SPG block, RFA and neuro-stimulation.  Studies included in this review were compiled and analyzed for their treated medical conditions, study design, outcomes and procedural details.  Studies were graded using Oxford Center for Evidence-Based Medicine for level of evidence.  Based on the level of evidence, grades of recommendations are provided for each intervention and its associated medical conditions.  A total of 83 publications were included in this review, of which 60 were studies on SPG block, 15 were on RFA, and 8 were on neuro-stimulation.  Of all the studies, 23 had evidence level above case series.  Of the 23 studies, 19 were on SPG block, 1 study on RFA, and 3 studies on neuro-stimulation.  The rest of the available literature was case reports and case series.  The strongest evidence lied in using SPG block, RFA and neuro-stimulation for CH; SPG block also had evidence in treating trigeminal neuralgia, migraines, reducing the needs of analgesics after endoscopic sinus surgery and reducing pain associated with nasal packing removal after nasal operations.  The authors concluded that SPG is a promising target for treating CH using blocks, RFA and neuro-stimulation; SPG block also had some evidence supporting its use in a few other conditions.  Moreover, they stated that most of the controlled studies were small and without replications; further controlled studies are needed to replicate and expand on these previous findings.

An UpToDate review on “Cluster headache: Treatment and prognosis” (May, 2018) states that “There are several promising but unproven methods using neurostimulation to treat medically refractory cluster headache, including sphenopalatine ganglion stimulation, occipital nerve stimulation, noninvasive vagus nerve stimulation, and deep brain stimulation.  All are investigational and require further study to confirm long-term benefit and safety”.

Sanchez-Gomez and colleagues (2018) evaluated the safety and effectiveness of peripheral neurostimulation of the SPG in the treatment of refractory CCH.  Various medical databases were used to perform a systematic review of the scientific literature.  The search for articles continued until October 31, 2016, and included clinical trials, systematic reviews and/or meta-analyses, health technology assessment reports, and clinical practice guidelines that included measurements of efficiency/effectiveness or adverse effects associated with the treatment.  The review excluded cohort studies, case-control studies, case series, literature reviews, letters to the editor, opinion pieces, editorials, and studies that had been duplicated or outdated by later publications from the same institution.  Regarding effectiveness, these investigators found that SPG stimulation had positive results for pain relief, attack frequency, medication use, and patients' QOL.  In the results regarding safety, these researchers found a significant number of AEs in the first 30 days following the intervention.  Removal of the device was necessary in some patients.  Little follow-up data, and no long-term data, were available.  The authors concluded that these findings are promising, despite the limited evidence available.  They considered it essential for research to continue into the safety and efficacy of SPG stimulation for patients with refractory CCH.  In cases where this intervention may be indicated, treatment should be closely monitored.

In sum, for individuals with episodic cluster headaches who receive transcutaneous VNS, the evidence includes randomized controlled trials (RCTs). One RCT for a cluster headache showed a reduction in headache frequency but did not include a sham treatment group. Two randomized, double-blind, sham-controlled studies showed efficacy of achieving pain-free status within 15 minutes of treatment with noninvasive VNS in patients with episodic cluster headaches but not in patients with chronic cluster headaches. The RCTs for episodic cluster headaches are promising, however, additional studies with larger relevant populations are required to establish the treatment efficacy. The evidence is insufficient to determine the effects of the technology on health outcomes. For individuals who have other neurologic, psychiatric, or metabolic disorders (e.g., epilepsy, depression, schizophrenia, noncluster headache, impaired glucose tolerance) who receive transcutaneous VNS, the evidence includes RCTs and case series for some of the conditions. Relevant outcomes are symptoms, change in disease status, and functional outcomes. The RCTs are all small and have various methodologic problems. None showed definitive efficacy of transcutaneous VNS in improving patient outcomes. The evidence is insufficient to determine the effects of the technology on health outcomes.
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Patwardhan RV, Stong B, Bebin EM, et al. Efficacy of vagal nerve stimulation in children with medically refractory epilepsy. Neurosurgery. Dec 2000;47(6):1353-1357; discussion 1357-1358. PMID 11126906

Premchand RK, Sharma K, Mittal S, et al. autonomic regulation therapy via left or right cervical vagus nerve stimulation in patients with chronic heart failure: results of the ANTHEM-HF trial. J Card Fail. Nov 2014;20(11):808-816. PMID 25187002

Puledda F, Goadsby PJ. Current approaches to neuromodulation in primary headaches: Focus on vagal nerve and sphenopalatine ganglion stimulation. Curr Pain Headache Rep. 2016 ;20(7):47.

Rush AJ, George MS, Sackeim HA, et al. Vagus nerve stimulation (VNS) for treatment-resistant depressions: a multicenter study. Biol Psychiatry. Feb 15 2000;47(4):276-286. PMID 10686262

Rush AJ, Marangell LB, Sackeim HA, et al. Vagus nerve stimulation for treatment-resistant depression: a randomized, controlled acute phase trial. Biol Psychiatry. Sep 1 2005;58(5):347-354. PMID 16139580

Ryvlin P, Gilliam FG, Nguyen DK, et al. The long-term effect of vagus nerve stimulation on quality of life in patients with pharmacoresistant focal epilepsy: the PuLsE (Open Prospective Randomized Long-term Effectiveness) trial. Epilepsia. Jun 2014;55(6):893-900. PMID 24754318

Sackeim HA, Rush AJ, George MS, et al. Vagus nerve stimulation (VNS) for treatment-resistant depression: efficacy, side effects, and predictors of outcome. Neuropsychopharmacology. Nov 2001;25(5):713-728. PMID 11682255

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Coding

Inclusion of a code in this table does not imply reimbursement. Eligibility, benefits, limitations, exclusions, precertification/referral requirements, provider contracts, and Company policies apply.

The codes listed below are updated on a regular basis, in accordance with nationally accepted coding guidelines. Therefore, this policy applies to any and all future applicable coding changes, revisions, or updates.

In order to ensure optimal reimbursement, all health care services, devices, and pharmaceuticals should be reported using the billing codes and modifiers that most accurately represent the services rendered, unless otherwise directed by the Company.

The Coding Table lists any CPT, ICD-9, ICD-10, and HCPCS billing codes related only to the specific policy in which they appear.

CPT Procedure Code Number(s)

MEDICALLY NECESSARY

61885, 61888, 64568, 64569, 64570, 95970, 95976, 95977

EXPERIMENTAL/INVESTIGATIONAL
0312T, 0313T, 0314T, 0315T, 0316T, 0317T

THE FOLLOWING CODES IS USED TO REPRESENT IMPLANTABLE VAGUS NERVE STIMULATION FOR CHRONIC HEART FAILURE
64999



Professional and outpatient claims with a date of service on or before September 30, 2015, must be billed using ICD-9 codes. Professional and outpatient claims with a date of service on or after October 1, 2015, must be billed using ICD-10 codes.

Facility/Institutional inpatient claims with a date of discharge on or before September 30, 2015, must be billed with ICD-9 codes. Facility/Institutional inpatient claims with a date of discharge on or after October 1, 2015, must be billed with ICD-10 codes.


ICD - 10 Procedure Code Number(s)

N/A


Professional and outpatient claims with a date of service on or before September 30, 2015, must be billed using ICD-9 codes. Professional and outpatient claims with a date of service on or after October 1, 2015, must be billed using ICD-10 codes.

Facility/Institutional inpatient claims with a date of discharge on or before September 30, 2015, must be billed with ICD-9 codes. Facility/Institutional inpatient claims with a date of discharge on or after October 1, 2015, must be billed with ICD-10 codes.


ICD -10 Diagnosis Code Number(s)

G40.011 Localization-related (focal) (partial) idiopathic epilepsy and epileptic syndromes with seizures of localized onset, intractable, with status epilepticus

G40.019 Localization-related (focal) (partial) idiopathic epilepsy and epileptic syndromes with seizures of localized onset, intractable, without status epilepticus

G40.111 Localization-related (focal) (partial) symptomatic epilepsy and epileptic syndromes with simple partial seizures, intractable, with status epilepticus

G40.119 Localization-related (focal) (partial) symptomatic epilepsy and epileptic syndromes with simple partial seizures, intractable, without status epilepticus

G40.211 Localization-related (focal) (partial) symptomatic epilepsy and epileptic syndromes with complex partial seizures, intractable, with status epilepticus

G40.219 Localization-related (focal) (partial) symptomatic epilepsy and epileptic syndromes with complex partial seizures, intractable, without status epilepticus

G40.311 Generalized idiopathic epilepsy and epileptic syndromes, intractable, with status epilepticus

G40.319 Generalized idiopathic epilepsy and epileptic syndromes, intractable, without status epilepticus

G40.411 Other generalized epilepsy and epileptic syndromes, intractable, with status epilepticus

G40.419 Other generalized epilepsy and epileptic syndromes, intractable, without status epilepticus

G40.803 Other epilepsy, intractable, with status epilepticus

G40.804 Other epilepsy, intractable, without status epilepticus

G40.813 Lennox-Gastaut syndrome, intractable, with status epilepticus

G40.814 Lennox-Gastaut syndrome, intractable, without status epilepticus

G40.823 Epileptic spasms, intractable, with status epilepticus

G40.824 Epileptic spasms, intractable, without status epilepticus

G40.89 Other seizures

G40.A11 Absence epileptic syndrome, intractable, with status epilepticus

G40.A19 Absence epileptic syndrome, intractable, without status epilepticus

G40.B11 Juvenile myoclonic epilepsy, intractable, with status epilepticus

G40.B19 Juvenile myoclonic epilepsy, intractable, without status epilepticus




HCPCS Level II Code Number(s)



MEDICALLY NECESSARY

L8679 Implantable neurostimulator, pulse generator, any type

L8680 Implantable neurostimulator electrode, each

L8681 Patient programmer (external) for use with implantable programmable neurostimulator pulse generator, replacement only

L8682 Implantable neurostimulator radiofrequency receiver

L8683 Radiofrequency transmitter (external) for use with implantable neurostimulator radiofrequency receiver

L8685 Implantable neurostimulator pulse generator, single array, rechargeable, includes extension

L8686 Implantable neurostimulator pulse generator, single array, non-rechargeable, includes extension

L8687 Implantable neurostimulator pulse generator, dual array, rechargeable, includes extension

L8688 Implantable neurostimulator pulse generator, dual array, non-rechargeable, includes extension

L8689 External recharging system for battery (internal) for use with implantable neurostimulator, replacement only

L8695 External recharging system for battery (external) for use with implantable neurostimulator, replacement only


EXPERIMENTAL/INVESTIGATIONAL

THE FOLLOWING CODE IS USED TO REPRESENT NON-IMPLANTABLE VAGUS NERVE STIMULATION DEVICES (E.G., GAMMACORE)

E1399 Durable medical equipment, miscellaneous



Revenue Code Number(s)

N/A

Coding and Billing Requirements


Cross References


Policy History

Revisions from 11.15.16n
01/21/2019This version of the policy is effective as of 01/21/2019.

Major update to this policy bulletin includes the following:

Non-implantable vagus nerve stimulation, (e.g., gammaCore™ [non-invasive vagus nerve stimulator (nVNS)]), is considered experimental/investigational and, therefore, not covered because the safety and/or effectiveness of this service cannot be established by review of the available published peer-reviewed literature in the treatment for conditions, including, but not limited to the following:
  • Epilepsy
  • Migraine headaches
  • Cluster headaches

  • Revisions from 11.15.16m
    01/01/2018This policy has been identified for the CPT code update, effective 01/01/2018.

    The following CPT code has been removed from this policy (out of scope): 64550


    Effective 10/05/2017 this policy has been updated to the new policy template format.


    Version Effective Date: 01/21/2019
    Version Issued Date: 01/22/2019
    Version Reissued Date: N/A

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