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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.
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Updated 03/2017