Pending Policies - Surgery


Surgical Deactivation of Headache Trigger Sites

Number:SUR712.031

Effective Date:02-15-2018

Coverage:

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Surgical deactivation of trigger sites is considered experimental, investigational and/or unproven for the treatment of migraine and non-migraine headache.

Radiofrequency ablation (thermal or pulse) is considered experimental, investigational and/or unproven for the treatment of occipital neuralgia.

Description:

Migraine Headache

Migraine is a common headache disorder with a prevalence in the United States (U.S.) of approximately 18% in women and 6% in men. (1) According to the International Headache Society, migraine headache is a recurrent disorder with attacks lasting 4 to 72 hours. Typical features of migraine headaches include unilateral location, pulsating quality, moderate or severe intensity, and associated symptoms such as nausea, photophobia, and/or phonophobia. (2)

Treatment Options

A variety of medications are used to treat acute migraine episodes. They include medications taken at the onset of an attack to abort the attack (triptans, ergotamines), and medications to treat the pain and other symptoms of migraines once they are established (nonsteroidal anti-inflammatory drugs, narcotic analgesics, antiemetics). Prophylactic medication therapy may be appropriate for people with migraines that occur more than 2 days per week. In addition to medication, behavioral treatments such as relaxation and cognitive therapy are used in the management of migraine headache. Moreover, botulinum toxin type A injections are a U.S. Food and Drug Administration (FDA) approved treatment for chronic migraine (migraines occurring on at least 15 days a month for at least 3 months).

Surgical deactivation of trigger sites is another proposed treatment of migraine headaches. The procedure was developed by plastic surgeon Bahman Guyuron, MD, following observations that some patients who had cosmetic forehead lifts often reported improvement or elimination of migraine symptoms postsurgery. (3, 4) The procedure is based on the theory that migraine headaches arise due to inflammation of trigeminal nerve branches in the head and neck caused by irritation of the surrounding musculature, bony foramen, and perhaps fascia bands. Accordingly, surgical treatment of migraines involves removing the relevant nerve sections, muscles, fascia, and/or vessels. The treatment is also based on the theory that there are specific migraine trigger sites and that these sites can be located in individual patients. In studies conducted by Guyuron’s research group, clinical evaluation and diagnostic injections of botulinum toxin have been used to locate trigger sites. The specific surgical procedure varies according to the patient’s migraine trigger site. The surgical procedures are performed under general anesthesia in an ambulatory care setting and take an average of 1 hour.

Surgical procedures have been developed at 4 trigger sites: frontal, temporal, rhinogenic, and occipital. Following is a description of each.

Frontal headaches are believed to be activated by irritation of the supratrochlear and suborbital nerves by glabellar muscles or vessels. The surgical procedure involves removal of the glabellar muscles encasing these nerves. Fat from the upper eyelid is used to fill the defect in the muscles and shield the nerve.

Temporal headaches may be activated by inflammation of the zygomatico-temporal branch of the trigeminal nerve by the temporalis muscles or vessels adjacent to the nerve. To treat migraines located at this trigger site, a segment (≈2.5 cm) of the zygomatico-temporal branch of the trigeminal nerve is removed endoscopically.

Rhinogenic headaches may involve intranasal abnormalities (e.g., deviated septum), which may irritate the end branches of the trigeminal nerve. Surgical treatment includes septoplasty and turbinectomy.

Occipital headaches may be triggered by irritation of the occipital nerve caused by the semispinalis capitis muscle or the occipital artery. Surgery consists of removal of a segment of the semispinalis capitis muscle medial to the greater occipital nerve approximately 1 cm wide and 2.5 cm long, followed by insertion of a subcutaneous flap between the nerve and the muscle to avoid nerve impingement.

Non-Migraine Headache

It has been proposed that other types of headaches (e.g., tension headaches) may also be triggered by irritation of the trigeminal nerve. Although this mechanism of action is less well established for headaches other than migraine, it is possible that surgical treatment of trigger sites may also be beneficial for some non?migraine headaches.

International Headache Society Classification Criteria for Headaches

Migraine without Aura

Recurrent headache disorder characterized by attacks lasting 4-72 hours.

Diagnostic Criteria

A. At least five attacks fulfilling criteria B-D.

B. Headache attacks lasting 4-72 hours (untreated or successfully treated).

C. At least 2 of the following 4 characteristics:

1. Unilateral location;

2. Pulsating quality;

3. Moderate or severe pain intensity;

4. Aggravation by or causing avoidance of routine physical activity (e.g. walking or climbing stairs).

D. During headache, at least 1 of the following:

1. Nausea and/or vomiting;

2. Photophobia and phonophobia.

E. Not better accounted for by another International Classification of Headache Disorders (ICHD-3) diagnosis.

Migraine with Aura

Recurrent attacks, lasting minutes, of unilateral fully reversible visual, sensory or other central nervous system symptoms that usually develop gradually and are usually followed by headache and associated migraine symptoms.

Diagnostic Criteria

A. At least 2 attacks fulfilling criteria B and C;

B. One or more of the following fully reversible aura symptoms:

1. Visual;

2. Sensory;

3. Speech and/or language;

4. Motor;

5. Brainstem;

6. Retinal.

C. At least 2 of the following 4 characteristics:

1. At least 1 aura symptom spreads gradually over ≥5 minutes, and/or 2 or more symptoms occur in succession;

2. Each individual aura symptom lasts 5-60 minutes;

3. At least 1 aura symptom is unilateral;

4. The aura is accompanied, or followed within 60 minutes, by headache.

D. Not better accounted for by another ICHD-3 diagnosis, and transient ischemic attack has been excluded.

Occipital Neuralgia

Occipital neuralgia is a relatively rare primary headache disorder (not caused by another condition) affecting around 3.2/100,000 people per year. The term “neuralgia” refers to pain in the distribution of a nerve, in this case, the occipital nerve(s). The greater, lesser, and third occipital nerves originate from the upper cervical nerve roots, course up the neck muscles, and exit near the base of the skull. These sensory nerves provide sensation to the back of the head, top of the head, and behind the ears. Pain originates from the occipital region and radiates along the course of the occipital nerves. The pain is episodic, brief, severe, and shock-like and may be triggered by routine activities such as moving the neck or wearing a hat. The cause of occipital neuralgia is unknown; however, entrapment and irritation of the nerves have been suspected. Pain secondary to trauma, such as whiplash injuries, inflammation, and compression of the occipital nerves by arteries or tumors have all been hypothesized, but no consensus has been reached. (5)

Treatment Options

Conservative management for occipital neuralgia includes warm compresses, massage, and physical therapy. Anti-inflammatory medications and muscle relaxers (e.g., baclofen) may provide relief of symptoms. Antiepileptic drugs (i.e., carbamazepine, gabapentin, pregabalin) and tricyclic antidepressants are often utilized to decrease the frequency and severity of attacks. When conservative measures are ineffective, occipital nerve blocks may be used for pain management. (5) For cases that are difficult to control, thermal or conventional radiofrequency ablation (RFA) has been proposed as a treatment modality. (5) In conventional or thermal RFA, a radiofrequency (RF) current is created which causes energy to pool in the tissue. This energy converts into heat which creates a small lesion on the nerve rendering it unable to transmit painful signals. pulsed RFA is similar, however, a higher voltage is used in a pulsing fashion, allowing the energy to dissipate more therefore, less heat is generated. This procedure leaves the nerve intact, while selectively “shocking” the A-delta and C fiber (pain conductors). (6)

Regulatory status

  • Surgical deactivation of headache triggers is a surgical procedure and, as such, is not subject to regulation by the U.S. FDA.
  • RFA is a procedure and, therefore, is not subject to regulation by the U.S. FDA. However, the devices used to perform RFA are regulated by the FDA premarket approval process. There are numerous devices listed in the FDA 510(k) database approved for RFA. Refer to the FDA web site at <https://www.fda.gov> for additional information on specific devices. Two product codes are dedicated to these devices: GXD for RF lesion generators (7) and GXI for RF lesion probes. Currently there are no RFA devices approved to treat occipital neuralgia. (8)

Rationale:

The medical policy was originally created in 2009 and has been updated regularly with searches of the MEDLINE database. The most recent literature review is through August 31, 2017.

Assessment of efficacy for a therapeutic intervention involves a determination of whether the intervention improves health outcomes. The optimal study design for this purpose is a randomized controlled trial (RCT) that includes clinically relevant measures of health outcomes. Headache research involves evaluating subjective outcomes (e.g., pain intensity, duration). As a result, blinded, sham-controlled, randomized trials are particularly important in determining efficacy above the placebo effect. Intermediate outcome measures (or surrogate outcome measures) may also be adequate if there is an established link between the intermediate outcome and true health outcomes. Nonrandomized comparative studies and uncontrolled studies can sometimes provide useful information on health outcomes but are prone to biases such as noncomparability of treatment groups, placebo effect, and variable natural history of the condition.

Migraine Headache

To date, 2 RCTs, from the same research group that includes the surgeon who developed the procedure (Guyuron), and 1 RCT from Iran have evaluated surgical deactivation of migraine headache trigger sites. A description of the RCTs is as follows.

An initial RCT assessing surgical deactivation of migraine trigger sites was published by Guyuron et al. in 2005; this trial was unblinded and did not include a sham control. (9) Eligibility included a diagnosis of migraine headache using International Classification of Headache Disorders II (ICHD-II) criteria. One hundred patients were assigned to the treatment group and 25 to the control group in a 4:1 allocation. They received up to 3 injections of botulinum toxin type A (Botox), 1 at each of their most common trigger sites, to identify a predominant site of headache trigger and potential response to treatment. To be considered candidates for surgery, patients had to have at least a 50% reduction in symptoms for 4 weeks after a botulinum toxin type A injection. Patients in the control group received saline injections instead of botulinum toxin and were ineligible for surgery; for the remainder of the treatment period, they received usual care. For patients in the intervention group, surgery varied by trigger site. In patients with predominantly frontal trigger migraine headache, the glabellar muscle group was removed to relieve compression of the supraorbital and supratrochlear nerves. Patients with temporal migraine headache underwent removal of 3 cm of the zygomatico-temporal branch of the trigeminal nerve. Patients with both temporal and frontal migraine headaches underwent both procedures. Patients with occipital migraine headache underwent removal of a portion of the semispinalis capitis muscles surrounding the occipital nerve, and a subcutaneous flap was used to shield the nerve from the muscle. Finally, patients with migraine headaches triggered from the septum and turbinates underwent septoplasty and inferior and/or middle turbinectomies.

Among patients assigned to the treatment group, 91 responded to botulinum toxin type A injection and underwent surgery and 89 (89%) of 100 completed the 12-month follow-up. There was differential dropout in the 2 groups: 19 (76%) of 25 patients in the control group were evaluated at 12 months. A total of 17 (14%) of 125 randomized patients were excluded from the analysis. In a per-protocol analysis at 12 months, 82 (92%) of 89 patients in the treatment group and 3 (16%) of 19 in the control group experienced significant improvement, defined as at least a 50% reduction in baseline migraine frequency, intensity, or duration. The difference between groups was statistically significant (p<0.001). Thirty-one (35%) of patients in the treatment group and none in the control group reported complete elimination of migraines. Most adverse events following surgery were minor and transient. The most commonly reported events were temporary nasal dryness (n=12) and rhinorrhea (n=11). Seven patients experienced intense scalp itching that lasted a mean of 6 months.

Five-year outcomes for patients in the treatment group were reported by Guyuron et al. in 2011. (10) Follow- up data were available for 79 patients (87% of those who underwent surgery, 79% of those randomized to the treatment group). Outcomes were reported for 69 patients. The other 10 had received additional migraine headache surgery and were excluded from the analysis. At 5 years, 20 (29%) of 69 reported complete elimination of migraine headache, 41 (59%) reported a significant decrease in symptoms, and 8 (12%) reported no significant change. All measured variables improved significantly at 5 years compared with baseline. For example, mean headache frequency per month decreased from 10.9 to 4.0 (p<0.001). Long-term data were not reported for patients assigned to the control group.

Limitations of the 2005 RCT include lack of blinding, lack of a sham-control, and randomization before determining eligibility for surgery. In addition, there is a potential cointervention bias: the surgery group but not the sham group received botulinum toxin injections, which may have had a therapeutic effect. Moreover, about 14% of patients were excluded from the analysis, which could have biased results. Furthermore, findings were not reported separately by surgical procedure. In terms of long-term follow-up, 5-year data were reported only for the treatment group.

In 2009, Guyuron et al. published a double-blind, sham-controlled trial evaluating surgical deactivation of migraine trigger sites in 76 patients. (3) Eligibility criteria included a diagnosis of migraine headache according to ICHD-II criteria (2) and headaches triggered from a single or predominant site, as determined by a headache diary and physical examination. Participants were then given an injection of botulinum toxin type A (Botox) at the prominent site from which migraine pain started. Patients who had a positive response to botulinum toxin type A (i.e., at least a 50% decrease in headache symptoms) and in whom headaches recurred after the effect of the botulinum toxin had disappeared were eligible for randomization. The methodology differed from that of the 2005 RCT (previously described), which randomized patients before receiving diagnostic botulinum toxin type A injections. In addition, in 2012, Liu et al. (Guyuron coauthored this study) further investigated the method of botulinum toxin injections to select patients for deactivation surgery and found that outcomes were similar in migraine surgery patients who did and did not undergo diagnostic Botox injections. (4) The Liu analysis raises questions about the need for the complex patient selection process used in the published RCTs.

In the 2009 RCT, participants were stratified by the predominant site from which headaches were triggered; frontal, temporal, or occipital, were randomized 2:1 to active or to sham surgery. A total of 317 participants were screened for inclusion; 130 received botulinum toxin type A injections and, based on responses to the injections, 76 were considered eligible for randomization. In each of the 3 active treatment groups, surgery consisted of exposure and removal of nerves and/or muscles. For patients in the sham group, surgery was limited to exposing the nerves and/or muscles; the integrity of the structures was left intact. The procedures differed according to the predominant headache trigger site and were similar to procedures used in the 2005 Guyuron trial. Briefly, patients in the frontal active surgery group underwent removal of the glabellar muscles encasing the supraorbital and supratrochlear nerves Patients in the temporal active surgery group underwent removal of a segment of the zygomaticotemporal branch of the trigeminal nerve. In the occipital surgery group, a segment of the semispinalis capitis muscle medial to the greater occipital nerve was removed.

Patients kept headache diaries and were seen at 3, 6, 9, and 12 months postsurgery. Seventy-five of 76 patients (49 in the active treatment group, 26 in the sham group) completed the 1-year follow-up. There were 29 patients in the frontal group (19 active treatment, 10 sham), 28 in the temporal group (19 active treatment, 9 sham), and 18 in the occipital group (11 active treatment, 7 sham). Patients remained blinded to their group assignment through 12 months, at which time patients in the sham surgery group were offered the surgical procedure. Key results are displayed in Table 1. Note that, for the frequency, intensity, and duration variables, there were no statistically significant differences by trigger site, so overall results are displayed. Results for the same outcomes from the 2005 Guyuron RCT are also summarized in Table 1.

Table 1. Summary of Outcomes for the Guyuron et al. Trials (2009, 2005)

Outcome Measures

Guyuron et al. (2009)3

Guyuron et al. (2005)9

Active Surgery (n=49)

Sham Surgery (n=26)

pb

Active Surgery (n=89)

Usual Care

(n=19)

pb

Completely eliminated headaches

28/49 (57.1%)

1/26 (3.8%)

<0.001

31/89 (35%)

0/19 (0%)

<0.001

Significant improvementa

41/49 (84%)

15/26 (58%)

0.005

82/89 (92%)

3/19 (16%)

<0.001

Mean headache frequency, month

0.005

Baseline (SD)

9.9 (6.0)

9.5 (4.4)

10.9 (0.8)

9.9 (1.7)

<0.001

12 months (SD)c

-7.4 (5.8)

-3.5 (5.4)

3.8 (0.4)

10.2 (1.7)

Mean headache intensity (1-10 VAS)

0.03

<0.001

Baseline (SD)

6.2 (1.7)

5.5 (1.4)

8.6 (0.13)

8.8 (0.24)

12 months (SD)c

-3.0 (3.5)

-1.3 (2.9)

4.0 (0.3)

7.0 (0.3)

Mean headache duration

0.43

0.007

Baseline (SD)

0.5 (0.6) d

1.7 (5.6) d

1.4 (0.14) h

1.3 (0.25) h

12 months (SD)c

-0.3 (0.5) d

-0.9 (4.5) d

0.4 (0.05) h

1.0 (0.2) h

Table Key: VAS: visual analog scale.

a Success was defined as at least a 50% reduction in the migraine index score at 12 months verses baseline.

b Between-group p values.

In the 2009 study, in addition to the between-group differences, there was statistically significant improvement in headache frequency, intensity, and duration from baseline to 12 months within the active surgery group and significant improvement in headache frequency and intensity within the sham surgery group. The improvement in outcomes within the sham group in the 2009 RCT were greater than those seen after usual care in the 2005 RCT, suggesting that there may be a substantial placebo effect associated with the surgery to deactivate trigger sites.

No adverse events were reported in the sham surgery group. All patients in the active treatment group reported some degree of paresthesia immediately after surgery. One patient experienced numbness 12 months after surgery. The most common adverse event in the active treatment group was temporal hollowing in 10 (53%) of 19 patients in the surgery group.

Advantages of the 2009 study included a sham control group and blinded comparison of outcomes in the 2 groups through 12 months postsurgery. Study limitations included small numbers of patients in each subgroup and a lack of reporting patients’ use of other migraine treatments (e.g., botulinum toxin type A, medications) during the 12-month follow-up. In addition, patient selection involved a long multicomponent selection process, which may be impractical on a widespread basis.

A 2014 review article critically evaluating the RCTs on surgical deactivation of migraine trigger sites included the following points (11):

The authors of the sham-controlled trial did not mention patients’ use of other headache treatments. Postoperative use of medications could have resulted in a reduction in headache frequency; these cases would have been counted as a surgical success in the study.

In the sham-controlled trial, baseline headache frequency was 9.9 migraines per month in the intervention group and 9.5 migraines per month in the control group and, therefore, the reduction of a small number of migraine episodes per month (which may not be clinically significant) could be considered a surgical success based on the author’s criterion of a 50% decrease in frequency.

Use of the terminology “migraine headaches per month” does not provide information on the number of days per month with migraine headaches or the number of non?migraine headaches per month.

Patients in the sham group may have guessed their group assignment because of retained movement of the corrugator supercilii, depressor supercilii, and procerus muscles. This could have biased their responses to subjective outcome questions.

Botulinum toxin type A (Botox) injections are a nonspecific screening tool and can lead to false positives when used to select patients for migraine surgery because Botox injections into the peripheral nerves may also modulate pain at central targets.

In 2016, Omranifard et al. published an RCT comparing surgical deactivation of migraine trigger sites to medical treatment in 50 patients from a single center in Iran. (12) The trial did not include a sham control and patients were not blinded to treatment group. All patients received injections of botulinum toxin into the frontal, temporal, and occipital trigger sites in a stepwise manner, with the most common site injected first. Investigators did not state how they evaluated patients’ responses to botulinum toxin or how their responses to botulinum toxin affected their eligibility to participate in the trial. Patients in the medical treatment group (n=25) were prescribed propranolol (80 mg daily) and amitriptyline (100 mg daily). Patients assigned to the surgery group (n=25) underwent decompression surgery in 1 or any combination of 4 trigger sites (frontal, temporal, septum, and/or occipital) they identified as relevant to their pattern of headaches. Surgical procedures were similar to those used in the Guyuron et al. RCTs except that a septal surgery option was added. For patients with frontal headaches, the glabellar muscles were removed. For patients with temporal headaches, a segment of the zygomaticotemporal branch of the trigeminal nerve was removed. For patients with occipital headaches, a segment of the semispinalis capitis muscle was removed, and the occipital artery was removed if it was entangled with the nerve. For patients with migraines originating at the septum, septoplasty and/or turbinectomy procedures were performed.

Trial findings are summarized in Table 2. All 12-month outcomes were significantly better in the surgery group compared with the medical treatment group. No adverse effects were reported. Interpreting trial findings is influenced by the lack of patient blinding, which raises concerns about subjective and patient-reported outcome measures. Results could be affected by the placebo effect. Moreover, it is not clear how patient outcomes data were collected (trialists did not mention patient diaries). Furthermore, surgeries differed by patient trigger sites, which makes it difficult to evaluate any particular surgical procedure.

Table 2. Summary of Outcomes for the Omranifard Trial (2016)

Outcome Measures

Omranifard et al. (2016)

Surgery (n=25)

Medical Treatment (n=25)

pb

Completely eliminated headaches, n/N (%)

9/25 (36%)

1/25 (4%)

<0.001

Success rate, n/N (%)a

19/25 (76%)

10/25 (40%)

<0.001

Mean headache frequency, month

<0.001

Baseline (SD)

15.9 (3.3)

15.2 (3.1)

12 months (SD)

6.4 (2.3)

10.5 (2.2)

Mean headache intensity (1-10 VAS)

0.001

Baseline (SD)

8.3 (0.3)

8.4 (0.3)

12 months (SD)

4.1 (0.2)

6.0 (0.2)

Mean headache duration, d

<0.001

Baseline (SD)

1.1 (0.5)

1.0 (0.4)

12 months (SD)

0.5 (0.3)

0.8 (0.3)

Table Key: VAS: visual analog scale.

a Success was defined as at least a 50% reduction in the migraine index score at 12 months verses baseline.

b Between-group p values.

Non-Migraine Headache

No studies were identified that evaluated surgical deactivation of trigger sites as a treatment of non-migraine headache.

Practice Guidelines and Position Statements

In 2013, the American Headache Society approved a list of 5 items that provide low value in headache medicine. (13) This list was produced as part of the American Board of Internal Medicine Foundation’s Choosing Wisely initiative. One of the 5 recommendations was: “Don’t recommend surgical deactivation of migraine trigger points outside of a clinical trial.” The 2013 document stated that the value of this procedure is still a research question and that large, multicenter randomized controlled trials with long- term follow-up are needed to provide accurate information on its benefits and harms.

Ongoing and Unpublished Clinical Trials

Some currently unpublished trials that might influence this review are listed in Table 3.

Table 3. Summary of Key Trials

NCT Number

Trial Name

Planned Enrollment

Completion Date

Ongoing

NCT02351544

Prospective, Multi-Center Evaluation of the Efficacy of Peripheral Trigger Decompression Surgery for Migraine Headaches

100

Sep 2018

Table Key: NCT: national clinical trial.

Section Summary: Surgical Deactivation for Headaches

Three RCTs have evaluated surgical deactivation of headache trigger sites. One RCT was double-blind and sham-controlled and the other 2 did not use a sham control or blind patients. All 3 trials reported statistically significantly better outcomes at 12 months in patients who received decompression surgery for migraine headache than the control intervention. However, the trials were subject to methodologic limitations (e.g., variability in surgical procedures, potential use of cointerventions, issues related to patient selection, outcome validation and measurement). In addition, in 2 of the 3 trials patients were unblinded and findings subject to the placebo effect. Furthermore, all 3 trials were single center and 2 were conducted by the same research group headed by the inventor of the procedure. Additional multicenter and sham-controlled randomized studies are needed.

For individuals who have migraine headaches who receive surgical deactivation of headache trigger sites, the evidence includes randomized controlled trials (RCTs). Relevant outcomes are symptoms, change in disease status, morbid events, and treatment-related morbidity. Three RCTs have been published; only 1 used a sham control and blinded patients to treatment group. All 3 trials reported statistically significantly better outcomes at 12 months in patients who received decompression surgery for migraine headache than the control intervention. However, the trials were subject to methodologic limitations (e.g., unclear and variable patient selection processes, variability in surgical procedures depending on trigger site). In addition, 2 of 3 trials were not blinded or sham-controlled and their findings are subject to the placebo effect. Additional sham-controlled randomized studies are needed. The evidence is insufficient to determine the effects of the technology on health outcomes.

For individuals who have non?migraine headaches who receive surgical deactivation of headache trigger sites, the evidence includes no published studies. Relevant outcomes are symptoms, change in disease status, morbid events, and treatment-related morbidity. The evidence is insufficient to determine the effects of the technology on health outcomes.

Occipital Neuralgia

No criterion standard has emerged for the treatment of occipital neuralgia. In 2010, Vanelderen et al. (14) evaluated the results of a prospective trial with 6 months of follow-up data where pulsed radiofrequency (RF) of the greater and/or lesser occipital nerve was used to treat occipital neuralgia. Patients presenting with clinical findings suggestive of occipital neuralgia and a positive test block of the occipital nerves with 2 mL of local anesthetic underwent a pulsed RFA of the culprit nerves. Mean scores for pain, quality of life, and medication intake were measured at 1, 2, and 6 months post procedure. Pain was measured by the visual analog and Likert scales, quality of life was measured by a modified brief pain questionnaire, and medication intake was measured by a Medication Quantification Scale. During a 29-month period, 19 patients were included in the study. Mean visual analog scale (VAS) and median Medication Quantification Scale scores declined by 3.6 units (P = 0.002) and 8 units (P = 0.006), respectively, during 6 months. Approximately 52.6% of patients reported a score of 6 (pain improved substantially) or higher on the Likert scale after 6 months. No complications were reported. The study concluded that pulsed RFA treatment of the greater and/or lesser occipital nerve is a promising treatment option for occipital neuralgia although further placebo-controlled trials are warranted.

In 2012 Huang and colleagues (15) aimed to provide outcome data evaluating pulsed RF for occipital neuralgia and to determine whether any demographic, clinical, or treatment characteristics are associated with success. The authors performed a retrospective data analysis on 102 subjects evaluating the effect of myriad factors on treatment success for occipital neuralgia and was conducted in academic civilian and military pain treatment centers. One hundred and two consecutive patients with a primary diagnosis of occipital neuralgia were treated with pulsed RF of the greater and/or lesser occipital nerve. A positive primary outcome was predefined as ≥50% pain relief lasting at least 3 months. The secondary outcome measure was procedural satisfaction. Fifty-two (51%) patients experienced ≥50% pain relief and satisfaction with treatment lasting at least 3 months. Variables associated with a positive outcome included a traumatic inciting event (65.7% success rate; P=0.03), lower diagnostic block volumes (odds ratio [OR]: 0.72; 95% confidence interval [CI]: 0.62-0.82; P<0.0001), and employment of multiple rounds of pulsed RF (OR: 2.95; 95% CI: 1.77-4.92; P<0.0001). Factors correlating with treatment failure included extension of pain anterior to the scalp apex (OR: 0.32; 95% CI: 0.14-0.73; P=0.006) and ongoing secondary gain issues (OR: 0.19; 95% CI: 0.11-0.33; P<0.0001). The study concluded pulsed RF may provide intermediate-term benefit in occipital neuralgia to a significant proportion of refractory cases. Careful attention to selection criteria and treatment parameters may further improve treatment outcomes.

In 2014, Ducic et al. (16) systematically compared the outcomes of different types of interventional procedures offered for the treatment of headaches and targeted toward peripheral nerves based on available published literature. A literature search of the Medline and Cochrane databases was performed. Relevant studies were selected by 2 independent reviewers and narrowed further by the application of predetermined inclusion and exclusion criteria. Studies were assessed for quality, and data were extracted regarding study characteristics (study type, level of evidence, type of intervention, and number of patients) and objective outcomes (success rate, length of follow-up, and complications). Pooled analysis was performed to compare success rates and complications between modality types. Of an initial 250 search results, 26 studies met the inclusion criteria. Of these, 14 articles studied nerve decompression, 9 studied peripheral nerve stimulation, and 3 studied RF intervention. When study populations and results were pooled, a total of 1253 patients had undergone nerve decompression with an 86% success rate, 184 patients were treated by nerve stimulation with a 68% success rate, and 131 patients were treated by RF with a 55% success rate. When compared to one another, these success rates were all statistically significantly different. Neither nerve decompression nor RF reported complications requiring a return to the operating room, whereas implantable nerve stimulators had a 31.5% rate of such complications. Minor complication rates were similar among all 3 procedures. Of the 3 most commonly encountered interventional procedures for chronic headaches, peripheral nerve surgery via decompression of involved peripheral nerves has been the best-studied modality in terms of total number of studies, level of evidence of published studies, and length of follow-up. Reported success rates for nerve decompression or excision tend to be higher than those for peripheral nerve stimulation or for RF, although poor study quantity and quality prohibit an accurate comparative analysis. Of the 3 procedures, peripheral nerve stimulator implantation was associated with the greatest number of complications. Although peripheral nerve surgery seems to be the interventional treatment modality that is currently best supported by the literature, better controlled and normalized high-quality studies are needed to better define the specific roles for each type of intervention.

In 2014, Manolitsis and Elahi (17) elected to perform an evidence-based review of the current literature through April 2013 concerning the use of pulsed RF for occipital neuralgia. The literature was reviewed at the Center for Pain Medicine and Regional Anesthesia, the University of Iowa Hospitals and Clinics. A total of 3 clinical studies and one case report investigating the use of pulsed RF for occipital neuralgia have been published worldwide. Statistically significant improvements in pain, quality of life, and adjuvant pain medication usage have been demonstrated. Clinical studies to date examining the efficacy of pulsed RF as a treatment for occipital neuralgia have yielded promising results, demonstrating sustained improvement in pain, quality of life, and adjuvant pain medication usage. The authors concluded, despite these encouraging clinical studies, conclusive evidence in support of pulsed RF as an interventional treatment option for occipital neuralgia awaits to be seen. Limitations of this study included lack of randomized control trials, small study sample sizes, an absence of diagnostic block imaging guidance, and the use of outcome measures that are inherently subjective, limiting objectivity and introducing an unquantifiable degree of bias.

In 2015, Cohen et al. (18) performed a multicenter, randomized, double-blind, comparative-effectiveness study in 81 participants with occipital neuralgia or migraine with occipital nerve tenderness whose aim was to determine which treatment is superior: steroid injections or pulsed RF. Forty-two participants were randomized to receive local anesthetic and saline, and three 120 second cycles of pulsed RF per targeted nerve, and 39 were randomized to receive local anesthetic mixed with deposteroid and 3 rounds of sham pulsed RF. Patients, treating physicians, and evaluators were blinded to interventions. The pulsed RF group experienced a greater reduction in the primary outcome measure, average occipital pain at 6 weeks (mean change from baseline -2.743 ± 2.487 vs -1.377 ± 1.970; P < 0.001), than the steroid group, which persisted through the 6-month follow-up. Comparable benefits favoring pulsed RF were obtained for worst occipital pain through 3 months (mean change from baseline -1.925 ± 3.204 vs -0.541 ± 2.644; P = 0.043), and average overall headache pain through 6 weeks (mean change from baseline -2.738 ± 2.753 vs -1.120 ± 2.1; P = 0.037). Adverse events were similar between groups, and few significant differences were noted for non-pain outcomes. The study concluded that although pulsed RF can provide greater pain relief for occipital neuralgia and migraine with occipital nerve tenderness than steroid injections, the superior analgesia may not be accompanied by comparable improvement on other outcome measures.

Ongoing and Unpublished Clinical Trials

There are no clinical trial publications that would influence this medical policy.

Practice Guidelines and Position Statements

The 2013 Institute for Clinical Systems Improvement's (ICSI) CPG Quality Standard (19), National Institute for Health and Clinical Excellence (NICE) Guidance on Headaches (20), and the 2017 American Association of Neurological Surgeons (AANS) (21) does not mention RFA as a treatment modality for occipital neuralgia

The 2016 American Headache Society (AHS) Evidence-Based Guidelines (22) for the Treatment of Cluster Headache: states “interventional therapies such as botox, sphenopalatine ganglion blockade, and RFA are available. RCTs carefully studying the safety and efficacy of these therapies are required before any specific recommendations can be made”

Section Summary: Occipital Neuralgia

The available evidence from published literature includes small randomized and small non-randomized studies and systemic reviews. The available evidence is limited and conflicting. Based on systematic reviews of thermal and pulsed radiofrequency ablation (RFA) for the treatment of occipital neuralgia, the randomized study did not provide strong evidence that RFA may be effective, where a few of the non-randomized studies suggested this technique may be effective. In summary, there is some evidence that radiofrequency (RF) techniques may offer a potential benefit, but this benefit has not been confirmed in adequate randomized controlled trials (RCTs) with sufficient sample size. Additional RCTs are needed with longer follow up and larger patient populations are needed to identify which patients would benefit from RFA. the available evidence from published studies is not sufficient to conclude that pulsed or thermal RFA is an effective treatment for occipital neuralgia therefore it is considered experimental, investigational, and/or unproven.

Contract:

Each benefit plan, summary plan description or contract defines which services are covered, which services are excluded, and which services are subject to dollar caps or other limitations, conditions or exclusions. Members and their providers have the responsibility for consulting the member's benefit plan, summary plan description or contract to determine if there are any exclusions or other benefit limitations applicable to this service or supply. If there is a discrepancy between a Medical Policy and a member's benefit plan, summary plan description or contract, the benefit plan, summary plan description or contract will govern.

Coding:

CODING:

Disclaimer for coding information on Medical Policies

Procedure and diagnosis codes on Medical Policy documents are included only as a general reference tool for each policy. They may not be all-inclusive.

The presence or absence of procedure, service, supply, device or diagnosis codes in a Medical Policy document has no relevance for determination of benefit coverage for members or reimbursement for providers. Only the written coverage position in a medical policy should be used for such determinations.

Benefit coverage determinations based on written Medical Policy coverage positions must include review of the member’s benefit contract or Summary Plan Description (SPD) for defined coverage vs. non-coverage, benefit exclusions, and benefit limitations such as dollar or duration caps.

CPT/HCPCS/ICD-9/ICD-10 Codes

The following codes may be applicable to this Medical policy and may not be all inclusive.

CPT Codes

15824, 15826, 30130, 30140, 30520, 64640, 64716, 64722, 64732, 64734, 64771, 64999, 64900

HCPCS Codes

None

ICD-9 Diagnosis Codes

Refer to the ICD-9-CM manual

ICD-9 Procedure Codes

Refer to the ICD-9-CM manual

ICD-10 Diagnosis Codes

Refer to the ICD-10-CM manual

ICD-10 Procedure Codes

Refer to the ICD-10-CM manual


Medicare Coverage:

The information contained in this section is for informational purposes only. HCSC makes no representation as to the accuracy of this information. It is not to be used for claims adjudication for HCSC Plans.

The Centers for Medicare and Medicaid Services (CMS) does not have a national Medicare coverage position. Coverage may be subject to local carrier discretion.

A national coverage position for Medicare may have been developed since this medical policy document was written. See Medicare's National Coverage at <http://www.cms.hhs.gov>.

References:

1. Bigal ME, Lipton RB. The epidemiology, burden, and comorbidities of migraine. Neurol Clin. May 2009; 27(2):321-334. PMID 19289218

2. Headache Classification Committee of the International Headache Society. The International Classification of Headache Disorders, 3rd edition (beta version). Cephalalgia. Jul 2013; 33(9):629-808. PMID 23771276

3. Guyuron B, Reed D, Kriegler JS, et al. A placebo-controlled surgical trial of the treatment of migraine headaches. Plast Reconstr Surg. Aug 2009; 124(2):461-468. PMID 19644260

4. Liu MT, Armijo BS, Guyuron B. A comparison of outcome of surgical treatment of migraine headaches using a constellation of symptoms versus botulinum toxin type A to identify the trigger sites. Plast Reconstr Surg. Feb 2012; 129(2):413-419. PMID 21987048

5. Holdridge A. American Migraine Foundation. Occipital neuralgia. 2016. Available at <https://americanmigrainefoundation.org> (accessed September 19, 2017)

6. Ainsworth Institute of Pain Management. Radiofrequency Ablation (RFA). 2016. Available at <http:// ainsworthinstitute.com> (accessed September 20, 2017)

7. FDA – Radiofrequency lesion generator (GXD). Food and Drug Administration – Center for Devices and Radiologic Health 2017. Available at <http://www.fda.gov> (accessed September 20, 2017).

8. FDA – Radiofrequency lesion probe (GXI). Food and Drug Administration – Center for Devices and Radiologic Health 2017. Available at <http://www.fda.gov> (accessed September 20, 2017).

9. Guyuron B, Kriegler JS, Davis J, et al. Comprehensive surgical treatment of migraine headaches. Plast Reconstr Surg. Jan 2005; 115(1):1-9. PMID 15622223

10. Guyuron B, Kriegler JS, Davis J, et al. Five-year outcome of surgical treatment of migraine headaches. Plast Reconstr Surg. Feb 2011; 127(2):603-608. PMID 20966820

11. Mathew PG. A critical evaluation of migraine trigger site deactivation surgery. Headache. Jan 2014; 54(1):142-152. PMID 24116941

12. Omranifard M, Abdali H, Ardakani MR, et al. A comparison of outcome of medical and surgical treatment of migraine headache: In 1 year follow-up. Adv Biomed Res. 2016; 5:121. PMID 27563631

13. Loder E, Weizenbaum E, Frishberg B, et al. Choosing wisely in headache medicine: the American Headache Society's list of five things physicians and patients should question. Headache. (Nov-Dec 2013); 53(10):1651-1659. PMID 24266337

14. Vanelderen P, Rouwette T, De Vooght P, et al. Pulsed radiofrequency for the treatment of occipital neuralgia: a prospective study with 6 months of follow-up. Reg Anesth Pain Med. Mar-Apr 2010; 35(2):148-51. PMID 20301822

15. Huang JH, Galvagno SM Jr, Hameed M, et al. Occipital nerve pulsed radiofrequency treatment: a multi-center study evaluating predictors of outcome. Pain Med (2012 Apr); 13(4):489-97. PMID 22390409

16. Ducic I, Felder JM 3rd, Fantus SA., et al. A systematic review of peripheral nerve interventional treatments for chronic headaches. Ann Plast Surg (2014 Apr); 72(4):439-45. PMID 24374395

17. Manolitsis N, Elahi F. Pulsed radiofrequency for occipital neuralgia. Pain Physician (2014 Nov-Dec); 17(6):E709-17. PMID 25415786

18. Cohen SP, Peterlin BL, Fulton L, et al. Randomized, double-blind, comparative-effectiveness study comparing pulsed radiofrequency to steroid injections for occipital neuralgia or migraine with occipital nerve tenderness. Pain (2015 Dec); 156(12):2585-94. PMID 26447705

19. Institute for Clinical Systems Improvement's CPG Quality Standard 42: Headache, Diagnosis and Treatment of (2013). Eleventh Edition. Available at <https://www.icsi.org> (accessed September 19, 2017)

20. National Institute For Health And Clinical Excellence (NICE). Headaches in over 12s: diagnosis and management. CG150 (September 19, 2012). Available at <www.nice.org.uk> (accessed September 20, 2017).

21. American Association of Neurological Surgeons. Occipital Neuralgia (2017). Available at <https://www.aans.org> (accessed September 18, 2017).

22. Robbins MS, Starling AJ, Pringsheim TM, Becker WJ, Schwedt TJ. Treatment of Cluster Headache: The American Headache Society Evidence-Based Guidelines. Headache (2016 Jul); 56(7):1093-106. PMID: 27432623

23. Surgical deactivation of headache trigger sites. Chicago, Illinois: Blue Cross Blue Shield Association Medical Policy Reference Manual (February 2017) Surgery 7.01.135.

Policy History:

Date Reason
2/15/2018 Document updated with literature review. The following was added to Coverage: Radiofrequency ablation (thermal or pulse) is considered experimental, investigational and/or unproven for the treatment of occipital neuralgia.
7/15/2017 Reviewed. No changes.
8/1/2016 Document updated with literature review. Coverage unchanged.
1/1/2015 Document updated with literature review. No change in overall coverage position. Title changed from Surgical Treatment of Cervicogenic Headache, Cranial Neuralgias or Variant of Migraine. CPT/HCPCS code(s) updated.
1/1/2012 Document updated with literature review. Coverage unchanged.
7/15/2009 New medical document

Archived Document(s):

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