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Number: 0707

Policy

*Please see amendment for Pennsylvania Medicaid at the end

of this CPB.

I. Aetna considers the following interventions experimental

and investigational for the treatment of cervicogenic

headache because their effectiveness for this indication has

not been established:

Botulinum toxin (however, botulinum toxin is considered

medically necessary for chronic migraine headache when

criteria in CPB 0113 ‐ Botulinum To xin (../100_199

/0113.html) are met)

C2 ganglion nerve block

Cryodenervation

Decompressive neck surgery

Electrical stimulation

Ganglionectomy

Local injections of anesthetics or corticosteroids

Radiofrequency denervation of cervical facet joints

Last Review 08/01/2016

Effective: 06/28/2005

Next Review: 08/27/2015

Review History

Definitions

Clinical Policy Bulletin Notes

II. Aetna considers the following interventions experimental

and investigational for the treatment of occipital

neuralgia and other types of headache because their

effectiveness for this indication has not been established:

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Auriculotemporal nerve block

Cervical rhizotomy

Cryodenervation

Decompression or microdecompression of the occipital

nerves

Dorsal column stimulation (see CPB 0194 ‐ Dorsal

Column Stimulation (../100_199/0194.html)) Electrical

stimulation of the occipital nerve (examples of

devices for occipital nerve stimulation are ONSTIM and

PRISM)

Ganglionectomy

Neurectomy

Neurolysis of the great occipital nerve with or without

section of the inferior oblique muscle

Neuroplasty

Occipital nerve block

Pulsed radiofrequency ablation (see CPB 0735 ‐ Pulsed

Radiofrequency)

Radiofrequency ablation/ radiofrequency denervation/

radiofrequency neurotomy

Resection or partial resection of muscle or tissue from

the forehead, peri‐orbital, occipital or other facial or

scalp areas

Resection or partial resection of the semispinalis capitus

muscle

Supraorbital nerve block

Suprascapular nerve block

Surgical release of the lesser occipital nerve within the

trapezius and other procedures to decompress occipital

nerves

Transection/avulsion of the occipital nerve

Thermal neurolysis (thermal and cryodenervation)

III. Aetna considers surgery and the following interventions

experimental and investigational for the treatment of cluster

headache and other chronic headaches including migraines

because their effectiveness for these indications has not

been established. Surgical interventions include some of the

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procedures listed below (not an all‐inclusive list):

Ablation or electrical stimulation of the sphenopalatine

ganglion (sphenopalatine ganglion block)

Bariatric surgery

Closure of patent foramen ovale

Decompression of the greater occipital, supra‐orbital and

supra‐trochlear nerves

Deep brain stimulation

Gamma knife (stereotactic) radiosurgery

Nerve decompression

Occipital nerve stimulation

Resection of the right and left supra‐orbital, supra‐

trochlear and infra‐trochlear nerves

Resection of musculature, including but not limited to the

corrugator supercilii muscle, or any soft tissue from the

forehead, peri‐orbital, occipital or other facial or scalp

areas; manipulation or repositioning of any muscle or

other soft tissue within these areas

Resection of any portion of the trigeminal nerve or its

branches

Sensory nerve decompression

Stellate ganglion block

Suboccipital nerve stimulation

Supraorbital nerve stimulation

Transposition of cranial sensory nerves

Vascular ligation of superficial extracranial arteries.

Note: For closure of patent foramen ovale for migraine

prophylaxis, see CPB 0292 ‐ Transcatheter Closure of Septal

Defects (../200_299/0292.html).

Background

A number of procedures or treatments have been proposed for

headaches and occipital neuralgia, including injections/blocks,

ablative techniques, occipital nerve stimulation, peripherally

implanted nerve stimulation or surgical procedures.

Injection therapy delivers local anesthetics, steroids or other

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agents into the region of the affected nerve(s) thereby reducing

pain and inflammation. Examples of injections/blocks used to

treat headaches or occipital neuralgia include, but may not be

limited to, occipital nerve block, greater occipital nerve block,

C2 ganglion nerve block, sphenopalantine nerve block, stellate

ganglion block, supraorbital nerve block or supratrochlear nerve

block.

Ablative procedures (eg, pulsed radiofrequency ablation,

radiofrequency ablation, radiofrequency denervation,

radiofrequency neurotomy, cryodenervation, neurolysis,

rhizotomy) may be performed in attempt to denervate the

occipital nerve (greater or lesser), upper cervical nerve (eg,

second cervical nerve, also known as C2), supraorbital,

supratrochlear or sphenopalatine ganglion. The proposed goal

of denervation is to "shut off" the pain signals that are sent to

the brain from the nerves. An additional purported objective is

to reduce the likelihood of, or to delay, any recurrence that may

occur by selectively destroying pain fibers without causing

excessive sensory loss, motor dysfunction or other

complications.

Surgical interventions are proposed as a treatment option to

relieve impingement of the nerve root(s) and thereby eliminate

symptoms caused by compression and injury to the cervical

nerves. Examples of surgical interventions include, but may not

be limited to, occipital nerve decompression,

microdecompression of the occipital nerve,

transection/avulsion of the occipital nerve, resection/partial

resection of the semispinalis capitus muscle, neuroplasty,

sensory nerve decompression, transposition of cranial sensory

nerve or ganglionectomy. Another surgical approach is vascular

ligation of superficial extracranial arteries (eg, superficial

branches of the external carotid artery, main trunk of the

superficial temporal artery, frontal branch of the superficial

temporal artery, occipital artery or posterior auricular artery)

which are theorized as an origin of headache pain in some

individuals.

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Cervicogenic Headache:

Cervicogenic headache (CGH) is a relatively common and still

controversial form of headache caused by disease or

dysfunction of structures in the cervical spine (e.g., congenital

anomalies of the cranio‐vertebral junction such as basilar

invagination, and atlanto‐axial dislocation; injury of the

ligaments, muscles, or joints of the neck). It can be triggered by

vascular or scar tissue compression of the C2 root and ganglion

as well as irritation of other upper cervical nerve roots (e.g., C3,

C4). In patients with CGH, attacks or chronic fluctuating periods

of neck/head pain may be provoked and/or worsened by

sustained neck movements or stimulation of ipsilateral tender

points. There are no diagnostic imaging techniques of the

cervical spine and associated structures that can determine the

exact source of pain. Although it has been advocated by some

headache clinicians that the use of nerve blocks is an important

confirmatory evidence for diagnosing CGH, the standardization

of diagnostic nerve blocks in the diagnosis of CGH remains to be

defined. Differential diagnoses of CGH include hemicrania

continua, chronic paroxysmal hemicrania, occipital neuralgia,

migraine headache and tension headache. Moreover, there is

considerable overlap in symptoms and findings between CGH

and migraine/tension headaches.

A curative treatment for CGH is unlikely to be developed until

the etiology of this disorder has been elucidated. Since CGH

appears to be refractory to common headache medication,

other treatments have been used in the management of CGH.

These entail non‐invasive therapies such as paracetamol and

non‐steroidal anti‐inflammatory drugs; manual modalities and

transcutaneous electrical nerve stimulation; local injections of

anesthetic, corticosteroids, or botulinum toxin type A (Botox);

as well as invasive surgical therapies such as decompression

and radiofrequency lesions of the involved nerve structures

(Jansen, 2000; Haldeman and Dagenais, 2001; Martelletti and

van Suijlekom, 2004).

In a Cochrane review, Langevin et al (2011) evaluated the

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literature on the treatment effectiveness of botulinum toxin

(BoNT) intra‐muscular injections for neck pain, disability, global

perceived effect and quality of life in adults with neck pain with

or without associated cervicogenic headache, but excluding

cervical radiculopathy and whiplash associated disorder. These

researchers included randomized and quasi‐randomized

controlled trials in which BoNT injections were used to treat

sub‐acute or chronic neck pain. A minimum of 2 review authors

independently selected articles, abstracted data, and assessed

risk of bias, using the Cochrane Back Review Group criteria. In

the absence of clinical heterogeneity, these

investigators calculated standardized mean differences (SMD)

and relative risks, and performed meta‐analyses using a

random‐effects model. The quality of the evidence and the

strength of recommendations were assigned an overall grade

for each outcome. They included 9 trials (503 subjects). Only

BoNT type A (BoNT‐A) was used in these studies. High quality

evidence suggested there was little or no difference in pain

between BoNT‐A and saline injections at 4 weeks (5 trials; 252

subjects; SMD pooled ‐0.07 (95 % confidence intervals ([CI]:

‐0.36 to 0.21)) and 6 months for chronic neck pain. Very low

quality evidence indicated little or no difference in pain

between BoNT‐A combined with physiotherapeutic exercise and

analgesics and saline injection with physiotherapeutic exercise

and analgesics for patients with chronic neck pain at 4 weeks (2

trials; 95 subjects; SMD pooled 0.09 [95 % CI: ‐0.55 to 0.73])

and 6 months (1 trial; 24 subjects; SMD ‐0.56 [95 % CI: ‐1.39 to

0.27]). Very low quality evidence from 1 trial (32 subjects)

showed little or no difference between BoNT‐A and placebo at 4

weeks (SMD 0.16 [95 % CI: ‐0.53 to 0.86]) and 6 months (SMD

0.00 [95 % CI: ‐0.69 to 0.69]) for chronic cervicogenic headache.

Very low quality evidence from 1 trial (31 subjects),

showed a difference in global perceived effect favouring BoNT‐A

in chronic neck pain at 4 weeks (SMD ‐1.12 [95 % CI: ‐1.89 to

‐0.36]). The authors concluded that current evidence fails to

confirm either a clinically important or a statistically significant

benefit of BoNT‐A injection for chronic neck pain associated

with or without associated cervicogenic headache. Likewise,

there was no benefit seen for disability and quality of life at 4

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week and 6 months.

In a review on CGH, Pollmann et al (1997) stated that neither

pharmacological nor surgical or chiropractic procedures lead to

a significant improvement or remission of CGH. These

investigators concluded that until controlled studies on large

and homogeneous groups of patients are performed, operative

intervention can not be recommended for CGH. Edmeads

(2001) noted that although expertly administered local

anesthetic blocks applied in a rational fashion can be of

diagnostic value, their value as treatment for CGH is much less

clear. Furthermore, Evers (2004) stated that for the

prophylactic treatment of migraine headache, tension

headache, and CGH, no sufficient positive evidence for

treatment with Botox is obtained from randomized, double‐

blind, placebo‐controlled trials to date.

Stovner et al (2004) reported on the results of a randomized,

double‐blind, placebo‐controlled study of radiofrequency

denervation of facet joints C2 through C6 in cervicogenic

headache. A total of 12 patients with disabling, long‐standing

and treatment‐resistant unilateral headache were randomly

assigned to receive either sham treatment or radiofrequency

neurotomy of facet joints C2 through C6 ipsilateral to the pain.

Patients were followed for 2 years by self‐assessed pain ratings,

measurements of sensitivity to pain and neck mobility

measurements for two years following treatment. The

investigators reported that subjects treated with neurotomy

were somewhat improved by 3 months after treatment, but

later there were no marked differences between groups. This

led the investigator to conclude that radiofrequency

denervation of cervical facet joints is probably not beneficial in

cervicogenic headache.

Occipital Neuralgia:

Occipital neuralgia, occurring more often in women than men,

is defined as a paroxysmal jabbing pain in the distribution of the

greater or lesser occipital nerves. It is characterized by pain in

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the cervical and posterior areas of the head that may/may not

radiate to the sides of the head as well as into the facial and

frontal areas. Occipital neuralgia can arise as a result of

compression of the greater or lesser occipital nerves, trauma

(e.g., whiplash), localized infections or inflammation, gout,

diabetes, blood vessel inflammation and local tumors. It may

occur as the nerves exit the trapezii or splenius muscle groups.

Compression of these nerves may result in a burning

dysasthesias in the occiput with or without radiation behind the

ear. Nerve compression can occur from cervical degeneration

or post‐traumatic compression of the C2 or C3 nerves. The

clinical features of the condition are pain and sensory change in

the distribution of the relevant nerve, localized nerve trunk

tenderness. Clinical signs and symptoms of occipital neuralgia

may also be produced by myofascial pain.

Treatments for occipital neuralgia ranges from rest, heat,

massage, exercise, antidepressants, nerve blocks, neurectomy,

cervical rhizotomy, surgical release of the occipital nerve within

the trapezius to neurolysis of the great occipital nerve with or

without section of the inferior oblique muscle. However, the

effectiveness of many of the invasive procedures has not been

firmly established.

Graff‐Radford (2001) stated that neurectomy has been

employed for occipital neuralgia, but the results are often

short‐lived. Barolat and Sharan (2000) stated that one of the

applications being developed for spinal cord stimulation is

occipital neuralgia.

Gille et al (2004) retrospectively evaluated a new surgical

treatment consisting of neurolysis of the great occipital nerve

and section of the inferior oblique muscle for the treatment of

greater occipital neuralgia (n = 10). All the patients had pain

exacerbated by flexion of the cervical spine. The average age of

the patients was 62 years. The mean follow‐up of the series

was 37 months. The results of the treatment were assessed

according to 3 criteria: (i) degree of pain on a visual analog

scale (VAS) before surgery, at 3 months, and at last follow‐up;

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(ii) consumption of analgesics before surgery and at follow‐up;

and (iii) the degree of patient satisfaction at follow‐up. In 3

cases, anatomic anomalies were found ‐‐ 1 patient had

hypertrophy of the venous plexus around C2; in another, the

nerve penetrated the inferior oblique muscle; the 3rd had

degenerative C1 to C2 osteoarthritis requiring associated C1 to

C2 arthrodesis. The mean VAS score was 80/100 before surgery

and 20/100 at last follow‐up. Consumption of analgesics

decreased in all patients. Seven of the 10 patients were very

satisfied or satisfied with the operation. The authors concluded

that the new surgical technique provided good results on

greater occipital neuralgia if patients are well chosen. The

findings by Gille et al (2004) were interesting, but they need to

be validated by prospective randomized controlled studies with

more patients.

There is a lack of evidence that local injection therapy such as

steroids, botulinum toxin and local anesthetics or surgical such

as decompression of the C2 nerve root, implantation of spinal

cord stimulator, neurolysis of the great occipital nerve and

surgical release of the occipital nerve within the trapezius

consistently provide sustained pain relief in the majority of

patients with CGH and occipital neuralgia. Furthermore, there

is also a lack of information regarding which patients might

obtain significant benefit from these procedures.

Recently, there has been increased interest in subcutaneous

electrical stimulation of the occipital nerve for the treatment of

occipital neuralgia. Kapural et al (2005) reported a case series

of 6 patients with severe occipital neuralgia who underwent

occipital nerve electrical stimulation lead implantation using a

modified midline approach. These patients had received

conservative and surgical therapies in the past including oral

anti‐depressants, membrane stabilizers, opioids, occipital nerve

blocks, and radiofrequency ablations. Significant decreases in

pain VAS scores and drastic improvement in functional capacity

were observed during the occipital stimulation trial and during

the 3‐month follow‐up after implantation. The mean VAS score

changed from 8.66 +/‐ 1.0 to 2.5 +/‐ 1.3 whereas pain disability

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index improved from 49.8 +/‐ 15.9 to 14.0 +/‐ 7.4. These

findings need to be validated by randomized controlled studies.

Electrical stimulation of the occipital nerve is also being

investigated for the treatment of chronic migraine headaches.

However, there is currently a lack of evidence regarding its

effectiveness for this indication.

Slavin et al (2006) analyzed records of 14 consecutive patients

(9 women and 5 men; mean age of 43.3 years) with intractable

occipital neuralgia (ON) treated with peripheral nerve

stimulation (PNS). Five patients had unilateral and 9 had

bilateral PNS electrodes inserted for trial, which was considered

successful if patient reported at least 50 % decrease of pain on

the visual analogue scale. Ten patients proceeded with system

internalization, and their long‐term results were analyzed. At

the time of the last follow‐up examination (5 to 32 months,

mean of 22 months), 7 patients (70 %) with implanted PNS

systems continue to experience beneficial effects of stimulation,

including adequate pain control, continuous employment, and

decrease in oral pain medications intake. Two patients had

their systems explanted because of loss of stimulation effect or

significant improvement of pain, and 1 patient had part of his

hardware removed because of infection. The authors

concluded that overall, the beneficial effect from chronic

stimulation in their series persisted in more than 50 % of the

patients for whom procedure was considered and in 80 % of

those who significantly improved during the trial and

proceeded with internalization. Thus, chronic PNS may be a

safe and relatively effective method for long‐term treatment of

chronic pain syndrome in patients with medically intractable

ON. The results of this small study are promising, but they need

to be validated by further investigation.

An interventional procedure consultation from the National

Institute for Health and Clinical Excellence (NICE, 2008)

concluded: "Current evidence on the safety and efficacy of

occipital nerve stimulation for intractable headache is

inadequate in both quantity and quality. Therefore this

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procedure should only be used with special arrangements for

clinical governance, consent and audit or research."

Kapural et al (2007) retrospectively described a series of 6

patients with severe occipital neuralgia who received

conservative and interventional therapies, including oral anti‐

depressants, membrane stabilizers, opioids, and traditional

occipital nerve blocks without significant relief. This group then

underwent occipital nerve blocks using the botulinum toxin

type A (BoNT‐A) Botox type A (50 U for each block; 100 U if

bilateral). Significant decreases in pain VAS scores and

improvement in Pain Disability Index (PDI) were observed at 4

weeks follow‐up in 5 out of 6 patients following BoNT‐A

occipital nerve block. The mean VAS score changed from 8 +/‐

1.8 (median score of 8.5) to 2 +/‐ 2.7 (median score of 1), while

PDI improved from 51.5 +/‐ 17.6 (median of 56) to 19.5 +/‐ 21

(median of 17.5) and the duration of the pain relief increased to

an average of 16.3 +/‐ 3.2 weeks (median of 16) from an

average of 1.9 +/‐ 0.5 weeks (median of 2) compared to

diagnostic 0.5 % bupivacaine block. Following block resolution,

the average pain scores and PDI returned to similar levels as

before BoNT‐A block. The authors concluded that BoNT‐A

occipital nerve blocks provided a much longer duration of

analgesia than diagnostic local anesthetics. The functional

capacity improvement measured by PDI was profound enough

in the majority of the patients to allow patients to resume their

regular daily activities for a period of time. This was a

retrospective, small study with short‐term follow‐up; its

findings need to be validated by well‐designed studies.

In a review on greater occipital nerve blockade, Selekler (2008)

stated that studies regarding greater occipital nerve injection in

primary headaches began with Michael Anthony and almost all

the studies today accept Anthony's studies as reference work.

Although more than 20 years had passed, there is insufficient

information about this procedure. According to available

evidence, steroids are apparently effective in both preventive as

well as therapy (for acute attack) in cluster headaches.

Effectiveness of occipital nerve blocks for the treatment

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of migraine headaches is not as dramatic as that observed

for cluster headaches. Despite the fact that local anesthetics

has a role in relieving acute attacks, single injection is

unsuitable as prophylasis. The authors concluded that although

there are case reports regarding the effectiveness of occipital

nerve blocks in relieving acute pain in cluster headaches and

migraine headaches, there is a need for systematized clinical

studies.

An American Headache Society Information Paper "Information

for Healthcare Professionals: Peripheral Nerve Blocks for

Headaches" (Robbins & Blumenfeld, 2012) provides descriptive

information about these blocks and includes three literature

citations (Ashkenazi & Levin, 2007; Ashkenazi, Blumenfeld, et al,

2010; Blumenfeld, Ashkenazi, et al., 2010). A review article by

Ashkenazi & Levin (2007) stated: “Several studies suggested

efficacy of GON [greater occipital nerve] block in the treatment

of migraine, cluster headache, and chronic daily headache.

However, few were controlled and blinded. Despite a favorable

clinical experience, little evidence exists for the efficacy of GON

block in migraine treatment. Controlled studies are needed to

better assess the role of GON block in the treatment of

migraine and other headaches. . . . Despite favorable clinical

experience, there is currently little convincing evidence for the

efficacy of GON block in the acute or preventive treatment of

headache. Most data on this topic come from non‐controlled

studies. Given the potentially high placebo effect that injections

to the head have on the degree of pain, these data should be

taken with reservation. Well‐designed controlled studies are

needed to better assess the role of GON block in headache

treatment, to determine the patient populations who would

benefit the most from this procedure, and to establish the

optimal drug combination to use for nerve blockade.”

The AHA Information Paper also cites Expert Consensus

Recommendations for the Performance of Peripheral Nerve

Blocks for Headaches (Blumenfeld & Ashkenazi, et al., 2010). As

the title suggests, this article focuses primarily on

recommendations on the proper performance of peripheral

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nerve blocks for headaches. Regarding the indications for

peripheral nerve blocks, the article refers readers to a literature

review by Ashkenazi, Blumenfeld, et al. (2010), which is

discussed below.

A literature review by Ashkenazi, Blumenfeld, et al. (2010), also

cited in the AHA Information Paper, concluded: “Our literature

review reveals paucity of controlled data on the efficacy of

PNBs and TPIs in headache management. Few studies have

addressed this issue, and the majority of those that did had

significant limitations, including a small number of patients, a

retrospective, non‐controlled design, and heterogeneous

groups of patients. In addition, the studies that have been done

so far differ in the technique used for nerve blockade, the type

and doses of local anesthetics used, the injected volume, the

location and number of injections, the time intervals between

injection sessions, and the way treatment efficacy was

assessed. Clearly, there is a need to obtain more data on the

efficacy of these treatments in the management of various

headache disorders in order to formulate a standardized

approach to their use in headache patients.” Specifically

regarding the effectiveness of occipital nerve blocks, the review

concluded: “The most widely examined procedure in this

setting was greater occipital nerve block, with the majority of

studies being small and non‐controlled.”

An editorial accompanying this systematic review (Blumenfeld

& Ashkenazi, Editorial, 2010) stated: “As the review article

demonstrates, however, there is a surprising paucity of

controlled studies to support the efficacy of these treatments

for headache. Moreover, the different studies reveal an

inconsistency in the methods used to block the targeted nerves;

the type of local anesthetics used, their doses, the volume of

injected drug, and even the location of injections have varied

considerably among the studies. While some investigators used

corticosteroids in addition to local anesthetics to block the

nerves, others did not. Clearly, there is a need for more work in

this area, and hopefully the articles in this issue will stimulate

additional interest and lead to the performance of larger and

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well‐controlled studies.”

Dach et al (2015) noted that several studies have presented

evidence that blocking peripheral nerves is effective for the

treatment of some headaches and cranial neuralgias, resulting

in reduction of the frequency, intensity, and duration of pain.

These investigators described the role of nerve block in the

treatment of headaches and cranial neuralgias, and the

experience of a tertiary headache center regarding this issue.

They also reported the anatomical landmarks, techniques,

materials used, contra‐indications, and side effects of

peripheral nerve block, as well as the mechanisms of action of

lidocaine and dexamethasone. The authors concluded that the

nerve block can be used in primary (migraine, cluster headache,

and nummular headache) and secondary headaches

(cervicogenic headache and headache attributed to

craniotomy), as well in cranial neuralgias (trigeminal

neuropathies, glossopharyngeal and occipital neuralgias). In

some of them this procedure is necessary for both diagnosis

and treatment, while in others it is an adjuvant treatment. The

block of the greater occipital nerve with an anesthetic and

corticosteroid compound has proved to be effective in the

treatment of cluster headache. Regarding the treatment of

other headaches and cranial neuralgias, controlled studies are

still needed to clarify the real role of peripheral nerve block.

An UpToDate review stated: "For patients with suspected

occipital neuralgia who have moderate to severe pain or

debilitating symptoms, we suggest a local occipital nerve block

(Grade 1B). This method can be both diagnostic and

therapeutic. Pain relief is typically prompt and may last several

weeks or even months. The procedure is generally safe and can

be repeated when pain recurs. Other causes for the

neuralgiform pain should be explored if occipital nerve block

fails."

Ducic et al (2009) presented the largest reported series of

surgical neurolysis of the greater occipital nerve in the

management of occipital neuralgia. A retrospective chart

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review was conducted to identify 206 consecutive patients

undergoing neurolysis of the greater or, less commonly, excision

of the greater and/or lesser occipital nerves. Pre‐operative and

post‐operative VAS and migraine headache indices were

measured. Success was defined as a reduction in pain of 50 %

or greater. Of 206 patients, 190 underwent greater occipital

nerve neurolysis (171 bilateral); 12 patients underwent greater

and lesser occipital nerve excision, whereas 4 underwent lesser

occipital nerve excision alone. The authors found that 80.5 % of

patients experienced at least 50 % pain relief and 43.4 % of

patients experienced complete relief of headache. Mean pre‐

operative pain score was 7.9 +/‐ 1.4. Mean post‐operative pain

was 1.9 +/‐ 1.8. Minimum duration of follow‐up was 12

months. There were 2 minor complications. The authors

concluded that neurolysis of the greater occipital nerve appears

to provide safe, durable pain relief in the majority of selected

patients with chronic headaches caused by occipital neuralgia.

The drawbacks of this study were the retrospective,

uncontrolled, and non‐blinded nature of the study.

Well‐designed studies are especially important for studying

interventions for pain, due to placebo effects, the waxing and

waning nature of the condition, and the potential effects of

other concurrent treatments on the person's pain.

In a prospective, randomized cross‐over study, Serra and

Marchioretto (2012) investigated the safety and effectiveness of

occipital nerve stimulation (ONS) for chronic migraine (CM) and

medication overuse headache (MOH) patients and evaluated

changes in disability, quality of life, and drug intake in implanted

patients. Eligible patients who responded to a

stimulation trial underwent device implantation and were

randomized to "Stimulation On" and "Stimulation Off" arms.

Patients crossed‐over after 1 month, or when their headaches

worsened. Stimulation was then switched On for all patients.

Disability as measured by the Migraine Disability Assessment

(MIDAS), quality of life (SF‐36), and drug intake (patient's diary)

were assessed over a 1‐year follow‐up. A total of 34 patients

(76 % women, 34 % men, mean age of 46 +/‐ 11 years) were

enrolled; 30 were randomized and 29 completed the study.

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Headache intensity and frequency were significantly lower in

the On arm than in the Off arm (p < 0.05) and decreased from

the baseline to each follow‐up visit in all patients with

Stimulation On (median MIDAS A and B scores: baseline = 70

and 8; 1‐year follow‐up = 14 and 5, p < 0.001). Quality of life

significantly improved (p < 0.05) during the study. Triptans and

non‐steroidal anti‐inflammatory drug use fell dramatically from

the baseline (20 and 25.5 doses/month) to each follow‐up visit

(3 and 2 doses/month at 1 year, p < 0.001). A total of 5 adverse

events occurred: 2 infections and 3 lead migrations. The

authors concluded that according to the results obtained, ONS

appears to be a safe and effective treatment for carefully

selected CM and MOH patients. The drawbacks of this study

were single‐center study, relatively small number of patients,

and absence of a control group. The authors stated that further

analyses on larger populations in multi‐center trials may

strengthen these promising findings.

Vadivelu et al (2012) reviewed retrospectively their experience

with ONS in patients with a primary diagnosis of Chiari

malformation and a history of chronic occipital pain intractable

to medical and surgical therapies. They presented a

retrospective analysis of 22 patients with Chiari malformation

and persistent occipital headaches who underwent occipital

neurostimulator trials and, after successful trials, permanent

stimulator placement. A trial was considered successful with

greater than 50 % pain relief as assessed with a standard VAS

score. Patients with a successful trial underwent permanent

placement approximately 1 to 2 weeks later. Patients were

assessed post‐operatively for pain relief via the VAS. Sixty‐eight

percent of patients (15 of 22) had a successful stimulator trial

and proceeded to permanent implantation. Of those

implanted, 87 % (13 of 15) reported continued pain relief at a

mean follow‐up of 18.9 months (range of 6 to 51 months).

Device‐related complications requiring additional surgeries

occurred in 40 % of patients. The authors concluded that ONS

may provide significant long‐term pain relief in selected Chiari I

malformation patients with persistent occipital pain. Moreover,

they stated that larger and longer‐term studies are needed to

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further define appropriate patient selection criteria and to

refine the surgical technique to minimize device‐related

complications.

Acar et al (2008) noted that surgical removal of the second (C2)

or third (C3) cervical sensory dorsal root ganglion is an option

to treat occipital neuralgia (ON). These investigators evaluated

the short‐term and the long‐term effectiveness of these

procedures for management of cervical and occipital

neuropathic pain. A total of 20 patients (mean age of 48.7

years) were identified who had undergone C2 and/or C3

ganglionectomies for intractable occipital pain and a

retrospective chart review undertaken. Patients were

interviewed regarding pain relief, pain relief duration, functional

status, medication usage and procedure satisfaction, pre‐

operatively, immediately post‐operative, and at follow‐up (mean

of 42.5 months). C2, C3 and consecutive ganglionectomies at

both levels were performed on 4, 5, and 11 patients,

respectively. All patients reported pre‐operative pain relief

following cervical nerve blocks. Average VAS scores were

9.4 pre‐operatively and 2.6 immediately after procedure.

Ninety‐five percent of patients reported short‐term pain relief

(less than 3 months). In 13 patients (65 %), pain returned after

an average of 12 months (C2 ganglionectomy) and 8.4 months

(C3 ganglionectomy). Long‐term results were excellent,

moderate, and poor in 20, 40 and 40 % of patients,

respectively. Cervical ganglionectomy offers relief to a majority

of patients, immediately after procedure, but the effect is short‐

lived. Nerve blocks are helpful in predicting short‐term success,

but a positive block result does not necessarily predict long‐

term benefit and therefore can not justify surgery by itself.

However, since 60 % of patients report excellent‐ moderate

results, cervical ganglionectomy continues to have a role in the

treatment of intractable ON. The findings of this small study

need to be validated by well‐designed studies.

Pisapia and colleagues (2012) examined the effectiveness of C2

nerve root decompression and C2 dorsal root ganglionectomy

for intractable ON and C2 ganglionectomy after pain recurrence

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following initial decompression. A retrospective review was

performed of the medical records of patients undergoing

surgery for ON. Pain relief at the time of the most recent

follow‐up was rated as excellent (headache relieved), good

(headache improved), or poor (headache unchanged or worse).

Telephone contact supplemented chart review, and patients

rated their pre‐operative and post‐operative pain on a 10‐point

numeric scale. Patient satisfaction and disability were also

examined. Of 43 patients, 29 (67 %) were available for follow‐

up after C2 nerve root decompression (n = 11), C2 dorsal root

ganglionectomy (n = 10), or decompression followed by

ganglionectomy (n = 8). Overall, 19 of 29 patients (66 %)

experienced a good or excellent outcome at most recent

follow‐up. Among the 19 patients who completed the

telephone questionnaire (mean follow‐up of 5.6 years), patients

undergoing decompression, ganglionectomy, or decompression

followed by ganglionectomy experienced similar outcomes,

with mean pain reduction ratings of 5 +/‐ 4.0, 4.5 +/‐ 4.1, and

5.7 +/‐ 3.5. Of 19 telephone responders, 13 (68 %) rated overall

operative results as very good or satisfactory. The authors

concluded that in the third largest series of surgical intervention

for ON, most patients experienced favorable post‐operative

pain relief. For patients with pain recurrence after C2

decompression, salvage C2 ganglionectomy is a viable surgical

option and should be offered with the potential for complete

pain relief and improved quality of life. Only 10 patients with C2

dorsal root ganglionectomy were available for follow‐up.

The moderate rate of follow‐up (67 %) may have skewed these

results.

Also, UpToDate reviews on “Occipital neuralgia” (Garza, 2012)

and “Cervicogenic headache” (Biondi and Bajwa, 2012) do not

mention the use of cryo‐denervation and ganglionectomy.

The supraorbital nerve is located on the front of the face over

the eyebrow. It supplies sensory innervation to the upper

eyelid, forehead, and scalp, extending almost to the lambdoidal

suture. A nerve block is a procedure in which an anesthetic

agent is injected directly near a nerve to block pain. It is a form

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of regional anesthesia.

Cluster Headache:

Cluster headaches are characterized by repeated attacks of

severe headache usually occurring several times a day. Patients

with chronic cluster headache have unremitting illness that

requires daily preventive medical treatment for years. Burns et

al (2007) examined the effectiveness of occipital nerve

stimulation (ONS) in the treatment of patients with refractory

chronic cluster headache (n = 8). Electrodes were implanted in

the suboccipital region for ONS. Other than the first patient,

who was initially stimulated unilaterally before being stimulated

bilaterally, all patients were stimulated bilaterally during

treatment. At a median follow‐up of 20 months (range of 6 to

27 months for bilateral stimulation), 6 of 8 patients reported

responses that were sufficiently meaningful for them to

recommend the treatment to similarly affected patients with

chronic cluster headache. Two patients noticed a substantial

improvement (90 % and 95 %) in their attacks; 3 patients

noticed a moderate improvement (40 %, 60 %, and 20 to 80 %,

respectively) and 1 reported mild improvement (25 %).

Improvements occurred in both frequency and severity of

attacks. These changes took place over weeks or months,

although attacks returned in days when the device

malfunctioned (e.g., with battery depletion). Adverse effects

were lead migrations in 1 patient and battery depletion

requiring replacement in 4. The authors concluded that ONS in

cluster headache seems to offer a safe, effective treatment

option that could begin a new era of neurostimulation therapy

for primary headache syndromes.

In a pilot study, Magis et al (2007) evaluated the effectiveness of

ONS in the treatment of patients with drug‐resistant chronic

cluster headache (drCCH). A total of 8 patients with drCCH had

a sub‐occipital neurostimulator implanted on the side of the

headache and were asked to record details of frequency,

intensity, and symptomatic treatment for their attacks in a diary

before and after continuous ONS. To detect changes in cephalic

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and extra‐cephalic pain processing, these researchers measured

electrical and pressure pain thresholds and the nociceptive

blink reflex. Two patients were pain‐free after a follow‐up of 16

and 22 months; 1 of them still had occasional autonomic

attacks. Three patients had around a 90 % reduction in attack

frequency. Two patients, 1 of whom had had the implant for

only 3 months, had improvement of around 40 %. Mean

follow‐up was 15.1 months (standard deviation of 9.5, range of

3 to 22 months). Intensity of attacks tends to decrease earlier

than frequency during ONS and, on average, is improved by 50

% in remaining attacks. All but 1 patient were able to

substantially reduce their preventive drug treatment.

Interruption of ONS by switching off the stimulator or because

of an empty battery was followed within days by recurrence

and increase of attacks in all improved patients. Occipital nerve

stimulation did not significantly modify pain thresholds. The

amplitude of the nociceptive blink reflex increased with longer

durations of ONS. There were no serious adverse events. The

authors concluded that ONS could be an efficient treatment for

drCCH and could be safer than deep hypothalamic stimulation.

The delay of 2 months or more between implantation and

significant clinical improvement suggests that the procedure

acts via slow neuromodulatory processes at the level of upper

brain stem or diencephalic centers.

In a retrospective analysis, Schwedt et al (2007) examined the

safety and effectiveness of ONS for medically intractable

headache. Pre‐ and post‐implantation data regarding headache

frequency, severity, disability, depression and post‐stimulator

complications were collected. A total of 15 patients (12 females

and 3 males) with age ranging from 21 to 52 years (mean of 39

years) were included in this study. Eight patients had chronic

migraine, 3 chronic cluster, 2 hemicrania continua and 2 had

post‐traumatic headache. Eight patients underwent bilateral

and 7 had unilateral lead placement. They were measured after

5 to 42 months (mean of 19 months). All 6 mean headache

measures improved significantly from baseline (p < 0.03).

Headache frequency per 90 days improved by 25 days from a

baseline of 89 days; headache severity (0 to 10) improved 2.4

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points from a baseline of 7.1 points; MIDAS disability improved

70 points from a baseline of 179 points; HIT‐6 scores improved

11 points from a baseline of 71 points; BDI‐II improved 8 points

from a baseline of 20 points; and the mean subjective percent

change in pain was 52 %. Most patients (60 %) required lead

revision within 1 year. One patient required generator revision.

The authors concluded that ONS may be effective in some

patients with intractable headache. Surgical revisions may be

commonly required. They noted that safety and effectiveness

results from prospective, randomized, sham‐controlled studies

in patients with medically refractory headache are needed to

validate these preliminary findings.

Jasper and Hayek (2008) noted that there is limited evidence

that ONS is a useful tool in the treatment of chronic severe

headaches. In a review on ONS for headache, Goadsby et al

(2008) stated that far from proven and with much work to be

done, neurostimulation therapy by means of ONS is an exciting

potential development for patients and doctors. Furthermore,

Trentman and Zimmerman (2008) stated that ONS may be an

effective minimally invasive treatment modality for refractory

headache disorders; however, further studies are needed.

Burns et al (2009) described the clinical outcome of ONS for 14

patients with intractable CCH. A total of 14 patients with

medically intractable CCH were implanted with bilateral

electrodes in the suboccipital region for ONS and a

retrospective assessment of their clinical outcome

wereobtained. At a median follow‐up of 17.5 months (range of

4 to 35 months), 10 of 14 patients reported improvement and 9

of these recommended ONS. Three patients noticed a marked

improvement of 90 % or better (90 %, 90 %, and 95 %,

respectively), 3 a moderate improvement of 40 % or better (40

%, 50 %, and 60 %, respectively), and 4 a mild improvement of

20 to 30% (20 %, 20 %, 25 %, and 30 %, respectively).

Improvement occurred within days to weeks for those who

responded most and patients consistently reported their

attacks returned within hours to days when the device was off.

One patient found that ONS helped abort acute attacks.

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Adverse events of concern were lead migrations and battery

depletion. The authors concluded that intractable CCH is a

devastating, disabling condition that has traditionally been

treated with cranially invasive or neurally destructive

procedures. Occipital nerve stimulation offers a safe, effective

option for some patients with CCH. However, they stated that

more work is needed to evaluate and understand this novel

therapy.

Narouze (2010) stated that cluster headache is a strictly

unilateral head pain that is associated with cranial autonomic

symptoms and usually follows circadian and circannual

patterns. Chronic cluster headache, which accounts for about

10 % to 15 % of patients with cluster headache, lacks the

circadian pattern and is often resistant to pharmacological

management. The sphenopalatine ganglion (SPG), located in

the pterygopalatine fossa, is involved in the pathophysiology of

cluster headache and has been a target for blocks and other

surgical approaches. Percutaneous radiofrequency ablation of

the SPG was shown to have encouraging results in those

patients with intractable cluster headaches.

Ansarinia et al (2010) examined the effects of electrical

stimulation of SPG for acute treatment of cluster headaches. A

total fo 6 patients with refractory CCH were treated with short‐

term (up to 1 hour) electrical stimulation of the SPG during an

acute cluster headaches. Headaches were spontaneously

present at the time of stimulation or were triggered with

agents known to trigger clusters headache in each patient. A

standard percutaneous infra‐zygomatic approach was used to

place a needle at the ipsilateral SPG in the pterygopalatine

fossa under fluoroscopic guidance.

Electrical stimulation was performed using a temporary

stimulating electrode. Stimulation was performed at various

settings during maximal headache intensity. Five patients had

cluster headaches during the initial evaluation. Three returned

3 months later for a second evaluation. There were 18 acute

and distinct cluster headache attacks with clinically maximal

VAS intensity of 8 (out of 10) and above. Electrical stimulation

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of SPG resulted in complete resolution of the headache in 11

attacks, partial resolution (greater than 50 % VAS reduction) in

3, and minimal to no relief in 4 attacks. Associated autonomic

features of cluster headache were resolved in each responder.

Pain relief was noted within several minutes of stimulation. The

authors concluded that SPG stimulation can be effective in

relieving acute severe cluster headache pain and associated

autonomic features. They stated that chronic long‐term

outcome studies are needed to determine the utility of SPG

stimulation for management and prevention of cluster

headaches.

In a prospective, cross‐over, double‐blind, multi‐center study,

Fontaine et al (2010) evaluated the safety and effectiveness of

unilateral hypothalamic deep brain stimulation (DBS) in 11

patients with severe refractory CCH. The randomized phase

compared active and sham stimulation during 1‐month periods,

and was followed by a 1‐year open phase. The severity of CCH

was assessed by the weekly attacks frequency (primary

outcome), pain intensity, sumatriptan injections, emotional

impact (HAD) and quality of life (SF12). Tolerance was assessed

by active surveillance of behavior, homeostatic and hormonal

functions. During the randomized phase, no significant change

in primary and secondary outcome measures was observed

between active and sham stimulation. At the end of the open

phase, 6/11 responded to the chronic stimulation (weekly

frequency of attacks decrease [50 %]), including 3 pain‐free

patients. There were 3 serious adverse events, including

subcutaneous infection, transient loss of consciousness and

micturition syncopes. No significant change in hormonal

functions or electrolytic balance was observed. Randomized

phase findings of this study did not support the effectiveness of

DBS in refractory CCH, but open phase findings suggested long‐

term effectiveness in more than 50 % patients, confirming

previous data, without high morbidity. Discrepancy between

these findings justifies additional controlled studies.

Other Headaches:

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Asensio‐Samper and colleagues (2008) presented the case of a

patient with headache because of post‐traumatic supra‐orbital

neuralgia, refractory to medical treatment, with good analgesic

control following peripheral nerve stimulation. The authors

stated that peripheral nerve stimulation may be considered a

safe, reversible treatment for patients with headache secondary

to supra‐orbital neuralgia who respond poorly to

pharmacological treatment, thus avoiding irreversible

alternatives such as surgery. Moreover, in a review on

neurostimulation in chronic cluster headache, Magis and

Schoenen (2008) noted that recent case reports

mentioned effectiveness of supra‐orbital and vagus nerve

stimulation. Whether these methods have a place in the

management of patients with intractable chronic cluster

headache remains to be determined.

Mathew (2009) stated that comparator studies that assess

treatment effects in a clinical setting have improved the

understanding of the efficacy and tolerability of prophylactic

treatments for chronic migraine. It is premature to recommend

device‐based treatments, such as ONS, vagal nerve stimulation,

and patent foramen ovale closure for chronic migraine, because

clinical trials are still in the preliminary stages.

Franzini et al (2009) stated that ONS is an emerging procedure

for the treatment of cranio‐facial pain syndromes and

headaches refractory to conservative treatments. Paemeleire

and Bartsch (2010) stated that ONS was originally described in

the treatment of occipital neuralgia. However, the spectrum of

possible indications has expanded in recent years to include

primary headache disorders, such as migraine and cluster

headaches. Retrospective and some prospective studies have

yielded encouraging results, and evidence from controlled

clinical trials is emerging. Moreover, these researchers noted

that ONS is far from a standardized technique at the moment.

They reviewed the recent literature on the topic, both with

respect to the procedure and its possible complications. An

important way to move forward in the scientific evaluation of

occipital nerve stimulation to treat refractory headache is the

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clinical phenotyping of patients to identify patients groups with

the highest likelihood to respond to this modality of treatment.

This requires multi‐disciplinary assessment of patients. The

development of occipital nerve stimulation as a new treatment

for refractory headache offers an exciting prospect to treat the

most disabled headache patients. Data from ongoing

controlled trials will shed new light on some of the unresolved

questions.

In a retrospective, descriptive study, Poggi et al (2008)

evaluated the effectiveness of surgical decompression of

multiple migraine trigger sites in a clinical practice setting, and

compared the results to those previously published. A total of

18 patients who had undergone various combinations of

surgical decompression of the supraorbital, supratrochlear, and

greater occipital nerves and zygomaticotemporal neurectomy

were included in this analysis. All patients had been diagnosed

with migraine headaches according to neurological evaluation

and had undergone identification of trigger sites by botulinum

toxin type A injections. Following surgical decompression, the

number of migraines per month and the pain intensity of

migraine headaches decreased significantly. Three patients (17

%) had complete relief of their migraines, and 9 of 18 (50 %)

had at least a 75 % reduction in the frequency, duration, or

intensity of migraines; and 39 % of patients have discontinued

all migraine medications. Mean follow‐up was 16 months

(range of 6 to 41 months) after surgery. All subjects stated they

would repeat the surgical procedure. The authors conclded that

the findings of this study supported the theory that peripheral

nerve compression triggers a migraine cascade. They verified a

reduction in duration, intensity, and frequency of migraine

headaches by surgical decompression of the supraorbital,

supratrochlear, zygomaticotemporal, and greater occipital

nerves. They stated that a significant amount of patient

screening is needed for proper patient selection and trigger site

identification for surgical success. These findings need to be

validated by well‐designed studies.

Kung et al (2011) stated that migraine headache can be a

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debilitating condition that confers a substantial burden to the

affected individual and to society. Despite significant

advancements in the medical management of this challenging

disorder, clinical data have revealed a proportion of patients

who do not adequately respond to pharmacologic intervention

and remain symptomatic. Recent insights into the pathogenesis

of migraine headache argue against a central vasogenic cause

and substantiate a peripheral mechanism involving compressed

craniofacial nerves that contribute to the generation of

migraine headache. Botulinum toxin injection is a relatively

new treatment approach with demonstrated efficacy and

supports a peripheral mechanism. Patients who fail optimal

medical management and experience amelioration of headache

pain after injection at specific anatomical locations can be

considered for subsequent surgery to decompress the

entrapped peripheral nerves. Migraine surgery is an exciting

prospect for appropriately selected patients suffering from

migraine headache and will continue to be a burgeoning field

that is replete with investigative opportunities. The authors

stated that future research will elucidate the anatomical

relationships of migraine trigger points and possibly identify

additional sites that have the capacities to generate migraines

... Research is currently being conducted to examine the

long‐term benefits of migraine surgery.

Magis and Schoenen (2011) reviewed the latest clinical trial

results in anti‐migraine treatment. The oral calcitonine gene‐

related peptide antagonist telcagepant is effective in acute

treatment. Compared to triptans, its effectiveness is almost

comparable but its tolerance is superior. The same is true for

the 5HT‐1F agonist lasmiditan. Triptans, as other drugs, are

more efficient if taken early but NSAIDs and analgesics remain

useful for acute treatment, according to several meta‐analyses.

Single‐pulse transcranial magnetic stimulation during the aura

rendered more patients pain‐free (39 %) than sham stimulation

(22 %) in 1 study. Topiramate could be effective for migrainous

vertigo, but it did not prevent transformation to chronic

migraine in patients with high attack frequency.

Onabotulinumtoxin A was effective for chronic

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migraine and well tolerated, but the therapeutic gain over

placebo was modest; the clinical profile of responders remains

to be determined before widespread use. Occipital nerve

stimulation was effective in intractable chronic migraine with 39

% of responders compared to 6 % after sham stimulation. This

and other neuromodulation techniques, such as sphenopalatine

ganglion stimulation, are promising treatments for medically

refractory patients; but large controlled trials are needed. One

study suggested that outcome of patent foramen ovale closure

in migraine might depend on anatomic and functional

characteristics.

In a prospective, observational study, Bond et al (2011)

examined if weight loss after bariatric surgery is associated with

improvements in migraine headaches. A total of 24 patients

who had migraine according to the ID‐Migraine screener were

assessed before and 6 months after bariatric surgery. At both

time points, patients had their weight measured and reported

on frequency of headache days, average headache pain

severity, and headache‐related disability over the past 90 days

via the Migraine Disability Assessment questionnaire. Changes

in headache measures and the relation of weight loss to these

changes were assessed using paired‐sample t tests and logistic

regression, respectively. Patients were mostly female (88 %),

middle‐aged (mean age of 39.3), and severely obese (mean

body mass index of 46.6) at baseline. Mean (+/‐ SD) number of

headache days was reduced from 11.1 +/‐ 10.3 pre‐operatively

to 6.7 +/‐ 8.2 post‐operatively (p < 0.05), after a mean percent

excess weight loss (% EWL) of 49.4 %. The odds of experiencing

a greater than or equal to 50 % reduction in headache days was

related to greater % EWL, independent of surgery type (p <

0.05). Reductions in severity were also observed (p < 0.05) and

the number of patients reporting moderate‐to‐severe disability

decreased from 12 (50.0 %) before surgery to 3 (12.5 %) after

surgery (p < 0.01). The authors concluded that severely obese

migraineurs experience marked alleviation of

headaches following significant weight reduction via bariatric

surgery. They stated that future studies are needed to

determine whether more modest, behaviorally produced

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weight losses can result in similar migraine improvements.

Limitations of this study included its observational nature, small

number of patients, and the lack of a control group. It would

also be interesting to determine if there is a dose‐response

relationship (i.e., whether greater weight loss results in greater

improvement).

Gaul et al (2011) noted that cluster headache is the most

common type of trigemino‐autonomic headache, affecting

approximately 120,000 persons in Germany alone. The attacks

of pain are in the peri‐orbital area on one side, last 90 minutes

on average, and are accompanied by trigemino‐autonomic

manifestations and restlessness. Most patients have episodic

cluster headache; about 15 % have chronic cluster headache,

with greater impairment of their quality of life. The attacks

often possess a circadian and seasonal rhythm. Oxygen

inhalation and triptans are effective acute treatment for cluster

attacks. First‐line drugs for attack prophylaxis include verapamil

and cortisone; alternatively, lithium and topiramate can be

given. Short‐term relief can be obtained by the subcutaneous

infiltration of local anesthetics and steroids along the course of

the greater occipital nerve, although most of the evidence in

favor of this is not derived from randomized clinical trials.

Patients whose pain is inadequately relieved by drug treatment

can be offered newer, invasive treatments, such as deep brain

stimulation in the hypothalamus (DBS) and bilateral ONS. The

authors concluded that pharmacotherapy for the treatment of

acute attacks and for attack prophylaxis is effective in most

patients. For the minority who do not gain adequate relief,

newer invasive techniques are available in some referral

centers. Definitive conclusions as to their value can not yet be

drawn from the available data.

The Work Loss Data Institute’s clinical guideline on “Neck and

upper back (acute & chronic)” (2011) listed greater occipital

nerve block (diagnostic and therapeutic) as one of the

interventions/procedures that are under study and are not

specifically recommended.

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The Institute for Clinical Systems Improvement's clinical practice

guideline on "Diagnosis and treatment of headache" (2011)

does not mention the use of decompression of the

occipital/greater occipital, supra‐orbital and supra‐trochlear

nerves. Furthermore, an UpToDate review on "Overview of

chronic daily headache" (Garza and Schwedt, 2012) does not

mention the use of decompression of the occipital, supra‐

orbital and supra‐trochlear nerves as a therapeutic option.

Saper et al (2011) presented preliminary safety and efficacy

data on ONS in patients with medically intractable CM. Eligible

subjects received an occipital nerve block, and responders were

randomized to adjustable stimulation (AS), pre‐set stimulation

(PS) or medical management (MM) groups. Seventy‐five of 110

subjects were assigned to a treatment group; complete diary

data were available for 66. A responder was defined as a

subject who achieved a 50 % or greater reduction in number of

headache days per month or a 3‐point or greater reduction in

average overall pain intensity compared with baseline.

Three‐month responder rates were 39 % for AS, 6 % for PS and

0 % for MM. No unanticipated adverse device events occurred.

Lead migration occurred in 12 of 51 (24 %) subjects. The

authors concluded that results of this feasibility study offer

promise and should prompt further controlled studies of ONS in

CM.

In an editorial that accompanied the afore‐mentioned study,

Schwedt (2011) stated that the findings by Saper et al

suggested that ONS is a promising treatment for CM and that

further clinical trials are needed. Schwedt noted several

drawbacks of the study ‐‐ (i) patients were taking migraine

prophylactic medications; the effects of these medications on

study results can not be determined, (ii) high complication rates

‐‐ 24 % of subjects had lead migration and 14 % had infection,

(iii) short‐term follow‐up ‐‐ this study only reported 3 months of

follow‐up; the need for battery replacement has to be

considered when discussing stimulator therapy, and (iv) only 39

% of subjects had benefits that met a priori criteria for

response. Schwedt stated that if ONS is to be considered a

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viable therapy, benefits must be persistent over a prolonged

duration of time with acceptable complication rated and

battery life.

Strand et al (2011) evaluated the effectiveness of a

microstimulator for chronic cluster headache. Four patients

with medically refractory chronic cluster headache underwent

implantation of a unilateral Bion microstimulator. In‐person

follow‐up was conducted for 12 months after implantation, and

a prospective follow‐up chart review was carried out to assess

long term outcome. Three of the participants returned their

headache diaries for evaluation. The mean duration of chronic

cluster headache was 14.3 years (range of 3 to 29 years). Pain

was predominantly or exclusively retro‐ocular/peri‐ocular. One

participant showed a positive response (greater than 50 %

reduction in cluster headache frequency) at 3 months post‐

implant, while there were 2 responders at 6 months. At least 1

of the participants continued to show greater than 60 %

reduction in headache frequency at 12 months. A chart review

showed that at 58 to 67 months post‐implant, all 3 participants

reported continued use and benefit from stimulation. No side‐

shift in attacks was noted in any participant. Adverse events

were limited to 2 participants with neck pain and/or cramping

with stimulation at high amplitudes; one required revision for a

faulty battery. The authors concluded that unilateral occipital

nerve stimulation, using a minimally invasive microstimulator,

may be effective for the treatment of medically refractory

chronic cluster headache. This benefit may occur immediately

after implantation, remain sustained up to 5 years after

implantation, and occur despite the anterior location of the

pain. They stated that prospective, randomized controlled trials

of occipital nerve stimulation (ONS) in chronic cluster headache

should proceed.

Lambru and Matharu (2012) stated that advances in the

management of headache disorders have meant that a

substantial proportion of patients can be effectively treated

with medical treatments. However, a significant minority of

these patients are intractable to conventional medical

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treatments. Occipital nerve stimulation is emerging as a

promising treatment for patients with medically intractable,

highly disabling chronic headache disorders, including migraine,

cluster headache and other less common headache

syndromes. Open‐label studies have suggested that this

treatment modality is effective and recent controlled trial data

are also encouraging. The procedure is performed using several

technical variations that have been reviewed along with the

complications, which are usually minor and tolerable. The

mechanism of action is poorly understood, though recent data

suggest that ONS could restore the balance within the impaired

central pain system through slow neuromodulatory processes in

the pain neuromatrix. While the available data are very

encouraging, the ultimate confirmation of the utility of a new

therapeutic modality should come from controlled trials before

widespread use can be advocated; more controlled data are still

needed to properly assess the role of ONS in the management

of medically intractable headache disorders. The authors

concluded that future studies also need to address the

variables that are predictors of response, including clinical

phenotypes, surgical techniques and stimulation parameters.

Presently, the Food and Drug Administration (FDA) has not

approved any device for ONS. Clinical trials are currently

underway for 2 ONS devices ‐‐ ONSTIM® (Medtronic Neuro) and

PRISM® (Boston Scientific Corporation) ‐‐ to ascertain the safety

and effectiveness of ONS for migraine headaches.

The Taiwan Headache Society’s treatment guidelines for “Acute

and preventive treatment of cluster headache” (Chen et al,

2011) evaluated both the acute and the preventive treatments

for cluster headache now being used in Taiwan, based on the

principles of evidence‐ based medicine. These investigators

assessed the quality of clinical trials and levels of evidence, and

referred to other treatment guidelines proposed by other

countries. Throughout several panel discussions, these

researchers merged opinions from the subcommittee members

and proposed a consensus on the major roles, recommended

levels, clinical efficacy, adverse events and cautions of clinical

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practice regarding acute and preventive treatments of cluster

headache. The majority of Taiwanese patients have episodic

cluster headaches, because chronic clusters are very rare.

Cluster headache is characterized by severe and excruciating

pain which develops within a short time and is associated with

ipsilateral autonomic symptoms. Therefore, emergency

treatment for a cluster headache attack is extremely

important. Within the group of acute medications currently

available in Taiwan, the subcommittee determined that high‐

flow oxygen inhalation has the best evidence of effectiveness,

followed by intra‐nasal triptans. Both are recommended as

1st‐line medical treatments for acute attacks. Oral triptans were

determined to be 2nd‐line medications. For transitional

prophylaxis, oral corticosteroids are recommended as the 1st‐

line medication, and ergotamine as the 2nd‐line choice. As for

maintenance prophylaxis, verapamil has the best evidence and

is recommended as the 1st‐line medication.

Lithium, melatonin, valproic acid, topiramate and gabapentin

are suggested as the 2nd‐line preventive medications. Surgical

interventions, including ONS, DBS, radiofrequency block of the

sphenopalatine ganglion, percutaneous radiofrequency

rhizotomy and trigeminal nerve section, are invasive and their

long‐term effectiveness and adverse events are still not clear in

Taiwanese patients; therefore, they are not recommended

currently by the subcommittee. The transitional and

maintenance prophylactic medications can be used together to

attain treatment effectiveness. Once the maintenance

prophylaxis achieves effectiveness, the transitional prophylactic

medications can be tapered gradually. The authors suggested

corticosteroids be used within 2 weeks, if possible. The

duration of maintenance treatment depends on the individual

patient's clinical condition, and the medications can be tapered

off when the cluster period is over.

Also, the National Clinical Guideline Centre’s guideline on

“Headaches: Diagnosis and management of headaches in young

people and adults” (NICE, 2012) as well as the Institute for

Clinical Systems Improvement’s clinical e guideline on

“Diagnosis and treatment of headache” (Beithon et al, 2013)

33 of 55

did not mention surgery as a therapeutic option.

Furthermore, an UpToDate review on “Chronic migraine” (Garza

and Schwedt, 2014) states that “Occipital nerve stimulation ‐‐

There are inconsistent data from small randomized trials

regarding the benefit of occipital nerve stimulation for the

treatment of chronic migraine. In the largest trial, there was no

significant difference at 12 weeks for the primary endpoint, the

percentage of patients that had a ≥ 50 percent reduction in

mean daily pain score in the active compared with the control

group. However, there were statistically significant if modest

improvements with active stimulation for a number of

secondary endpoints, including the percentage of patients with

a ≥ 30 percent reduction in mean daily pain score, and

reduction in the mean number of headache days and migraine‐

related disability. The findings from these reports are limited

by concerns about blinding in the control (sham treatment)

groups, given that active treatment causes paresthesia, and

relatively high rates of complications, including lead migration

in 14 to 24 percent of subjects. Further trials are needed to

determine if occipital nerve stimulation is a useful therapy for

chronic migraine”. This review also does not mention the use of

surgical interventions as therapeutic options.

Lip and Lip (2014) identified the extent of patent foramen ovale

prevalence in migraineurs and examined if closure of a patent

foramen ovale would improve migraine headache. An

electronic literature search was performed to select studies

between January 1980 and February 2013 that were relevant to

the prevalence of patent foramen ovale and migraine, and the

effects of intervention(s) on migraine attacks. Of the initial 368

articles presented by the initial search, 20 satisfied the inclusion

criteria assessing patent foramen ovale prevalence in

migraineurs and 21 presented data on patent foramen ovale

closure. In case series and cohort studies, patent foramen

ovale prevalence in migraineurs ranged from 14.6 % to 66.5 %.

Case‐control studies reported a prevalence ranging from 16.0 %

to 25.7 % in controls, compared with 26.8 % to 96.0 % for

migraine with aura. The extent of improvement or resolution of

34 of 55

migraine headache attack symptoms varied. In case series,

intervention ameliorated migraine headache attack in 13.6 % to

92.3 % of cases. One single randomized trial did not show any

benefit from patent foramen ovale closure. The overall data did

not exclude the possibility of a placebo effect for resolving

migraine following patent foramen ovale closure. The authors

concluded that this systematic review demonstrated firstly that

migraine headache attack is associated with a higher

prevalence of patent foramen ovale than among the general

population. Moreover, observational data suggested that some

improvement of migraine would be observed if the patent

foramen ovale were to be closed. They stated that a proper

assessment of any interventions for patent foramen ovale

closure would require further large randomized trials to be

conducted given uncertainties from existing trial data.

Ashkenazi et al (2010) stated that interventional procedures

such as peripheral nerve blocks (PNBs) and trigger point

injections (TPIs) have long been used in the treatment of

various headache disorders. There are, however, little data on

their efficacy for the treatment of specific headache syndromes.

Moreover, there is no widely accepted agreement among

headache specialists as to the optimal technique of injection,

type, and doses of the local anesthetics used, and injection

regimens. The role of corticosteroids in this setting is also

debated. These researchers performed a PubMed search of the

literature to find studies on PNBs and TPIs for headache

treatment. They classified the abstracted studies based on the

procedure performed and the treated condition. They found

few controlled studies on the efficacy of PNBs for headaches,

and virtually none on the use of TPIs for this indication. The

most widely examined procedure in this setting was greater

occipital nerve block, with the majority of studies being small

and non‐controlled. The techniques, as well as the type and

doses of local anesthetics used for nerve blockade, varied

greatly among studies. The specific conditions treated also

varied, and included both primary (e.g., migraine, cluster

headache) and secondary (e.g., cervicogenic, post‐traumatic)

headache disorders. Trigeminal (e.g., supra‐orbital) nerve

35 of 55

blocks were used in few studies. Results were generally

positive, but should be taken with reservation given the

methodological limitations of the available studies. The

procedures were generally well‐tolerated. The authors

concluded that there is a need to perform more rigorous clinical

trials to clarify the role of PNBs and TPIs in the management of

various headache disorders, and to aim at standardizing the

techniques used for the various procedures in this setting.

The Institute for Clinical Systems Improvement’s clinical

guideline on “Diagnosis and treatment of headache” (ICSI,

2013) did not mention trigeminal nerve block as a therapeutic

option.

Giblin et al (2014) described a case of cervicogenic headache

with associated autonomic features and pain in a trigeminal

distribution, all of which responded to 3rd occipital nerve

radiofrequency ablation. This study discussed the case of a 38‐

year old woman with history of migraines and motor vehicle

accident. Right third occipital nerve diagnostic blocks and

radiofrequency lesioning were carried out. Outcome measures

included pain reduction; physical findings, including periorbital

and mandibular facial swelling, tearing, conjunctival injection,

and allodynia; and use of opioid and non‐opioid pain medicines.

The patient had complete relief of her pain and

autonomic symptoms, and was able to stop all pain medications

following a dedicated third occipital nerve lesioning. The

authors concluded that this case illustrated the diagnostic and

therapeutic complexity of cervicogenic headache and the

overlap with other headache types, including trigeminal

autonomic cephalgias and migraine. It represented a unique

proof of principle in that not only trigeminal nerve pain but also

presumed neurogenic inflammation can be relieved by

blockade of cervical nociceptive inputs. They stated that further

investigation into shared mechanisms of headache pathogenesis

is warranted.

36 of 55

CPT Codes / ICD‐10 Codes / HCPCS Codes

Informa'tion in the [brackets] below has been added for

clarifica'tion purposes. Codes requiring a 7th character are

represented by "+":

Cervicogenic, cluster and other chronic headaches:

CPT codes not covered for indications listed in the CPB:

Ganglionectomy :

No specific code

14040 Adjacent tissue transfer or rearrangement, forehead,

cheeks, chin, mouth, neck, axillae, genitalia, hands

and/or feet; defect 10 sq cm or less

14041 defect 10.1 sq cm to 30.0 sq cm

14060 Adjacent tissue transfer or rearrangement, eyelids,

nose, ears and/or lips; defect 10 sq cm or less

14061 defect 10.1 sq cm to 30.0 sq cm

15824 Rhytidectomy; forehead

15826 Rhytidectomy; glabellar frown lines

43631 ‐ Gastrectomy, partial, distal, or vagotomy when

43635 performed with partial distal gastrectomy

43644 ‐ Laparoscopy, surgical gastric restrictive procedure

43645 [gastric bypass]

43770 ‐ Laparoscopy, surgical gastric restrictive procedure

43775 [gastric restrictive device]

43842 ‐ Gastric restrictive procedure, without gastric bypass,

43848 for morbid obesity, or gastric restrictive procedure

with partial gastrectomy, pylorus‐preserving

duodenoileostomy and ileoileostomy (50 to 100 cm

common channel) to limit absorption (biliopancreatic

diversion with duodenal switch), or gastric restrictive

procedure, with gastric bypass for morbid obesity, or

revision, open, of gastric restrictive procedure for

morbid obesity, other than adjustable gastric

restrictive device (separate procedure)

37 of 55

43886 ‐

43888

Gastric restrictive procedure, open

61796 Stereotactic radiosurgery (particle beam, gamma ray,

or linear accelerator); 1 simple cranial lesion

[auriculotemporal nerve block]

+61797 each additional cranial lesion, simple (List

separately in addition to code for primary procedure)

[auriculotemporal nerve block]

+61798 1 complex cranial lesion [auriculotemporal nerve

block]

+61799 each additional cranial lesion, complex (List

separately in addition to code for primary procedure)

[auriculotemporal nerve block]

+61800 Application of stereotactic headframe for

stereotactic radiosurgery (List separately in addition

to code for primary procedure) [auriculotemporal

nerve block]

61850 Twist drill or burr hole(s) for implantation of

neurostimulator electrodes, cortical

61860 Craniectomy or craniotomy for implantation of

neurostimulator electrodes, cerebral, cortical

61863 Twist drill, burr hole, craniotomy, or craniectomy

with stereotactic implantation of neurostimulator

electrode array in subcortical site (e.g. thalamus,

globus pallidus, subthalamic nucleus, periventrical,

periaqueductal gray, without use of intraoperative

microelectrode recording; first array

+61864 each additional array (List separately in addition to

primary procedure)

61867 Twist drill, burr hole, craniotomy, or craniectomy

with stereotactic implantation of neurostimulator

electrode array in subcortical site (e.g. thalamus,

globus pallidus, subthalamic nucleus, periventrical,

periaqueductal gray, with use of intraoperative

microelectrode recording; first array

38 of 55

+61868 each additional array (List separately in addition to

primary procedure)

61870 Craniectomy for implantation of neurostimulator

electrodes, cerebellar; cortical

61880 Revision or removal of intracranial neurostimulator

electrode

61885 Insertion or replacement of cranial neurostimulator

pulse generator or receiver, direct or inductive

coupling; with connection to a single electrode array

61886 Incision and subcutaneous placement of cranial

neurostimulator pulsed generatory or receiver, direct

or inductive coupling; with connection to two or

more electrode arrays

61888 Revision or removal of cranial neurostimulator pulse

generator or receiver

62280 Injection/infusion of neurolytic substance, with or

without other therapeutic substance; subarachnoid

62281 Injection/infusion of neurolytic substance, with or

without other therapeutic substance; epidural,

cervical or thoracic

63020 Laminotomy (hemilaminectomy), with

decompression of nerve root(s), including partial

facetectomy, foraminotomy and/or excision of

herniated intervertebral disc, including open and

endoscopically‐assisted approaches; 1 interspace,

cervical

+ 63035 each additional interspace, cervical or lumbar (List

separately in addition to code for primary procedure)

63040 Laminotomy (hemilaminectomy), with

decompression of nerve root(s), including partial

facetectomy, foraminotomy and/or excision of

herniated intervertebral disc, reexploration, single

interspace; cervical

+ 63043 each additional cervical interspace (List separately

in addition to code for primary procedure)

39 of 55

63045 Laminectomy, facetectomy and foraminotomy

(unilateral or bilateral with decompression of spinal

cord, cauda equina and/or nerve root(s), (e.g., spinal

or lateral recess stenosis)), single vertebral segment;

cervical

+ 63048 each additional segment, cervical, thoracic, or

lumbar (List separately in addition to code for

primary procedure)

63050 Laminoplasty, cervical, with decompression of the

spinal cord, two or more vertebral segments

63075 Discectomy, anterior, with decompression of spinal

cord and/or nerve root(s), including

osteophytectomy; cervical, single interspace

+ 63076 cervical, each additional interspace (List separately

in addition to code for primary procedure)

63077 thoracic, single interspace

63081 Vertebral corpectomy (vertebral body resection),

partial or complete, anterior approach with

decompression of spinal cord and/or nerve root(s);

cervical, single segment

+ 63082 cervical, each additional segment (List separately

in addition to code for primary procedure)

64400 Injection, anesthetic agent; trigeminal nerve, any

division or branch

64402 facial nerve

64405 greater occipital nerve

64408 vagus nerve

64410 phrenic nerve

64413 cervical plexus

64418 suprascapular nerve

64550 Application of surface (transcutaneous)

neurostimulator

64553 Percutaneous implantation of neurostimulator

electrodes; cranial nerve

40 of 55

64555 Percutaneous implantation of neurostimulator

electrodes; peripheral nerve (excludes sacral nerve)

64565 Percutaneous implantation of neurostimulator

electrodes; neuromuscular

64568 Incision for implantation of cranial nerve (eg, vagus

nerve) neurostimulator electrode array and pulse

generator

64575 periphereal nerve (excludes sacral nerve)

64580 Incision for implantation of neurostimulator

electrodes; neuromuscular

64585 Revision or removal of peripheral neurostimulator

electrodes

64590 Insertion or replacement of peripheral or gastric

neurostimulator pulse generator or receiver, direct or

inductive coupling

64702 ‐

64727

Neuroplasty digital, or major peripheral nerve, arm

or leg, open, or neuroplasty and/or transposition, or

decompression, unspecified nerve, or internal

neurolysis, requiring use of operating microscope

64600 Destruction by neurolytic agent, trigeminal nerve;

supraorbital, infraorbital, mental, or inferior alveolar

branch

64612 Chemodenervation of muscle(s); muscle(s)

innervated by facial nerve, unilateral (eg, for

blepharospasm, hemifacial spasm)

64616 neck muscle(s), excluding muscles of the larynx,

unilateral (eg, for cervical dystonia, spasmodic

torticollis)

64633 Destruction by neurolytic agent, paravertebral facet

joint nerve(s) with imaging guidance (fluoroscopy or

CT); cervical or thoracic, single facet joint

64634 cervical or thoracic, each additional facet joint (List

separatelyin addition to code for primary procedure)

64640 Destruction by neurolytic agent; other peripheral

nerve or branch

41 of 55

64716 Neuroplasty and/or transposition; cranial nerve

(specify

64732 Transection or avulsion of; supraorbital nerve

64734 Transection or avulsion of; infraorbital nerve

64744 Transcection or avulsion of; greater occipital nerve

64771 Transection or avulsion of other cranial nerve,

extradural [trigeminal nerve or its branches]

67900 Repair of brow ptosis (supraciliary, mid‐forehead or

coronal approach)

77371 Radiation treatment delivery, stereotactic

radiosurgery (SRS), complete course of treatment of

cranial lesion(s) consisting of 1 session; multi‐source

Cobalt 60 based

77372 linear accelerator based

77432 Stereotactic radiation treatment management of

cranial lesion(s) (complete course of treatment

consisting of one session)

93580 Percutaneous transcatheter closure of congenital

interatrial communication (ie, Fontan fenestration,

atrial septal defect) with implant

95970 Electronic analysis of implanted neurostimulator

pulse generator system (e.g. rate, pulse amplitude

and duration, configuration of wave form, battery

status, electrode selectability, output modulation,

cycling, impedamce and patient compliance

measurements); simple or complex brain, spinal

cord, or peripheral (i.e., cranial nerve, peripheral

nerve, autonomic nerve, neuromuscular)

neurostimulator pulse generator/transmitter,

without reprogramming

95971 simple brain, spinal cord, or peripheral (i.e.,

peripheral nerve, autonomic nerve, neuromuscular)

neurostimulator pulse generator/transmitter, with

intraoperative or subsequent programming

42 of 55

95972 complex spinal cord, or peripheral (ie, peripheral

nerve, sacral nerve, neuromuscular) (except cranial

nerve) neurostimulator pulse generator/transmitter,

with intraoperative or subsequent programming

95974 Electronic analysis of implanted neurostimulator

pulse generator system (e.g. rate, pulse amplitude

and duration, configuration of wave form, battery

status, electrode selectability, output modulation,

cycling, impedance and patient compliance

measurements); complex cranial nerve

neurostimulator, pulse generator/transmitter, with

intraoperative or subsequent programming, with or

without nerve interface testing, first hour

+95975 complex cranial nerve neurostimulator pulse

generator/transmitter, with intraoperative or

subsequent programming, each additional 30

minutes after first hour (List separately in addition to

code for primary procedure)

95978 Electronic analysis of implanted neurostimulator

pulse generator system (e.g. rate, pulse amplitude

and duration, battery status, electrode selectability,

and polarity, impedance and patient compliance

measurements); complex deep brain

neurostimulator pulse generator/transmitter, with

initial or subsequent programming, first hour

+95979 each additional 30 minutes after first hour (List

separately in addition to code for primary procedure)

97014 Application of a modality to 1 or more areas;

electrical stimulation (unattended

HCPCS codes not covered for indications listed in the CPB:

A4556 Electrodes (e.g., apnea monitor), per pair

A4557 Lead wires (e.g., apnea monitor), per pair

A4558 Conductive gel or paste, for use with electrical device

(e.g., TENS, NMES)

A4595 Electrical stimulator supplies, 2 lead, per month (e.g.,

TENS, NMES)

43 of 55

C1767 Generator, neurostimulator (implantable),

nonrechargeable

C1778 Lead, neurostimulator (implantable)

C1816 Receiver and/or transmitter, neurostimulator

(implantable)

C1883 Adaptor/extension, pacing lead or neurostimulator

lead (implantable)

C1897 Lead, neurostimulator test kit (implantable)

E0720 Transcutaneous electrical nerve stimulation (TENS)

device, 2 lead, localized stimulation

E0730 Transcutaneous electrical nerve stimulation (TENS)

device, 4 or more leads for multiple nerve

stimulation

E0731 Form‐fitting conductive garment for delivery of TENS

or NMES (with conductive fibers separated from the

patient's skin by layers of fabric)

E0745 Neuromuscular stimulator, electronic shock unit

G0173 Linear accelerator based stereotactic radiosurgery,

complete course of therapy in one session

G0251 Linear accelerator based stereotactic radiosurgery,

delivery including collimator changes and custom

plugging, fractionated treatment, all lesions, per

session, maximum five sessions per course of

treatment

G0339 Image‐guided robotic linear accelerator‐based

stereotactic radiosurgery, complete course of

therapy in one session or first session of fractionated

treatment

G0340 Image‐guided robotic linear accelerator‐based

stereotactic radiosurgery, delivery including

collimator changes and custom plugging,

fractionated treatment, all lesions, per session,

second through fifth sessions, maximum five sessions

per course of treatment

J0585 Botulinum toxin type A, per unit

44 of 55

J0587 Botulinum toxin type B, per 100 units

J0588 Injection, Incobotulinumtoxin A, 1 unit

L8679 Implantable neurostimulator, pulse generator, any

type

L8680 Implantyable 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

ICD‐10 codes not covered for indications listed in the CPB:

G43.001 ‐

G43.919

Migraine

G44.001 ‐

G44.89

Other headache syndromes

R51 Headache

Occipital neuralgia:

CPT codes not covered for indications listed in the CPB:

45 of 55

There is no specific code for Ganglionectomy:

62280 Injection/infusion of neurolytic substance, with or

without other therapeutic substance; subarachnoid

62281 Injection/infusion of neurolytic substance, with or

without other therapeutic substance; epidural,

cervical or thoracic

63185 Laminectomy with rhizotomy; 1 or 2 segments

63190 more than 2 segments

63650 Percutaneous implantation of neurostimulator

electrode array, epidural

63655 Laminectomy for implantation of neurostimulator

electrodes, plate/paddle, epidural

63661 Removal of spinal neurostimulator electrode

percutaneous array(s), including fluoroscopy, when

performed

63662 Removal of spinal neurostimulator electrode

plate/paddle(s) placed via laminotomy or

laminectomy, including fluoroscopy, when performed

63663 Revision including replacement, when performed, of

spinal neurostimulator electrode percutaneous

array(s), including fluoroscopy, when performed

63664 Revision including replacement of spinal

neurostimulator electrode plate/paddle(s) placed via

laminotomy or laminectomy, including fluoroscopy,

when performed

63685 Insertion or replacement of spinal neurostimulator

pulse generator or receiver, direct or inductive

coupling

63688 Revision or removal of implanted spinal

neurostimulator pulse generator or receiver

64405 Injection, anesthetic agent; greater occipital nerve

64555 Percutaneous implantation of neurostimulator

electrodes; peripheral nerve (excludes sacral)

64744 Transection or avulsion of; greater occipital nerve

46 of 55

64802 Sympathectomy, cervical

64804 Sympathectomy, cervicothoracic

95970 Electronic analysis of implanted neurostimulator

pulse generator system (e.g., rate, pulse amplitude

and duration, configuration of wave form, battery

status, electrode selectability, output modulation,

cycling, impedance and patient compliance

measurements); simple or complex brain, spinal

cord, or peripheral (i.e., cranial nerve, peripheral

nerve, autonomic nerve, neuromuscular)

neurostimulator pulse generator/transmitter,

without reprogramming

95971 simple spinal cord, or peripheral (i.e., peripheral

nerve, autonomic nerve, neuromuscular)

neurostimulator pulse generator/transmitter, with

intraoperative or subsequent programming

HCPCS codes not covered for indications listed in the CPB:

C1778 Lead, neurostimulator (implantable)

C1816 Receiver and/or transmitter, neurostimulator

(implantable)

E0745 Neuromuscular stimulator, electronic shock unit

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

47 of 55

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

ICD‐10 codes not covered for indications listed in the CPB:

M54.81 Occipital neuralgia

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AETNA BETTER HEALTH® OF PENNSYLVANIA

Amendment to Aetna Clinical Policy Bulletin Number: 0707

Headaches: Invasive Procedures

There are no amendments for Medicaid.

www.aetnabetterhealth.com/pennsylvania

Updated 03/2017