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Pain Medicine 2014; 15: 473–478
Wiley Periodicals, Inc.
HEADACHE & FACIAL PAIN SECTION
Case Report
Headache Plus: Trigeminal and Autonomic
Features in a Case of Cervicogenic Headache
Responsive to Third Occipital Nerve
Radiofrequency Ablation
Kathryn Giblin, MD, Jordan L. Newmark, MD,
Gary J. Brenner, MD, PhD, and
Brian J. Wainger, MD, PhD
Massachusetts General Hospital, Boston,
Massachusetts, USA
Reprint requests to: Gary J. Brenner, MD, PhD and
Brian J. Wainger, MD, PhD, Department of Anesthesia,
Critical Care and Pain Medicine, Massachusetts
General Hospital, WACC 340, Boston, MA 02114,
USA. Tel: 313-588-0270; Fax: 617-726-3441; E-mail:
gjbrenner@partners.org and bwainger@partners.org.
Conflict of interest/disclosures: None.
Abstract
Objective. To describe a case of cervicogenic
headache with associated autonomic features and
pain in a trigeminal distribution, all of which
responded to third occipital nerve radiofrequency
ablation.
Design. Single case report.
Setting. Massachusetts General Hospital Center for
Pain Medicine.
Patients. A 38-year-old woman with history of
migraines and motor vehicle accident.
Interventions. Right third occipital nerve diagnostic
blocks and radiofrequency lesioning.
Outcome Measures. Pain reduction; physical
findings, including periorbital and mandibular
facial swelling, tearing, conjunctival injection, and
allodynia; and use of opioid and non-opioid
pain medicines.
Results. The patient had complete relief of her pain
and autonomic symptoms, and was able to stop all
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pain medications following a dedicated third occipi-
tal nerve lesioning.
Conclusions. This case illustrates the diagnostic
and therapeutic complexity of cervicogenic head-
ache and the overlap with other headache types,
including trigeminal autonomic cephalgias and
migraine. It represents a unique proof of principle in
that not only trigeminal nerve pain but also pre-
sumed neurogenic inflammation can be relieved by
blockade of cervical nociceptive inputs. Further
investigation into shared mechanisms of headache
pathogenesis is warranted.
Key Words. Cervicogenic Headache; Trigeminal
Autonomic Cephalgia; Radiofrequency Ablation;
Third Occipital Nerve
Introduction
In cervicogenic headache, pain is classically present in
the occipital, parietal, and auricular regions innervated by
cervical nerves, but can also occur in the frontal and
orbital regions subserved by the V1 branch of the tri-
geminal nerve. Anatomically, the basis of cervicogenic
headache is in the spinal trigeminocervical complex,
where the spinal trigeminocervical nucleus receives con-
vergent primary nociceptive inputs from both cervical
(C1, C2, and C3) and trigeminal (V1 spinal tract) sensory
afferents, and then gives rise to the second-order
ascending trigeminothalamic tract [1]. Due to this dual
input from C1–C3 and V1 onto the second-order noci-
ceptive neurons, cervical pathology can result in referred
pain in cervical and occipital as well as trigeminal distri-
butions, including the dura. This wide distribution of
referred pain has been validated experimentally. For
example, noxious focal stimulation with hypertonic saline
of cervical structures innervated by C1, C2, and C3, such
as the suboccipital and posterior cervical muscles,
atlanto-occipital, lateral atlanto-axial, and C2–C3
zygapophysial joints, elicits occipital, parietal, frontal, and
orbital pain [2,3]. The greater occipital nerve arises from
473
Giblin et al.
Table 1 International Classification of Headache
Disorders 3rd edition (ICHD-3) (beta) criteria
11.2.1: Cervicogenic Headache
A. Any headache fulfilling criterion C
B. Clinical, laboratory, and/or imaging evidence of a
disorder or lesion within the cervical spine or soft
tissues of the neck, known to be able to cause
headache
C. Evidence of causation demonstrated by at least two of
the following:
1. Headache has developed in temporal relation to the
onset of the cervical disorder or appearance of the
lesion.
2. Headache has significantly improved or resolved in
parallel with improvement in or resolution of the
cervical disorder or lesion.
3. Cervical range of motion is reduced and headache
is made significantly worse by provocative
maneuvers.
4. Headache is abolished following diagnostic
blockade of a cervical structure or its nerve supply.
D. Not better accounted for by another ICHD-3 diagnosis
the medial branch of the dorsal ramus of C2, while the
third occipital nerve (TON) stems from the medial branch
of the dorsal ramus of C3 and runs superficially. The
C2–C3 zygapophyseal joint is innervated predominantly
by the TON, along with articular branches from the C2
dorsal ramus and infrequently with modest inner-
vation from the greater occipital nerve. The C3–C4
zygapophyseal joint is innervated by the deep portion of
the C3 medial branch, after it gives off the TON, as well
as the C4 medial branch [4].
Although the pathophysiological basis for cervicogenic
headache has been well elucidated, particularly in com-
parison to other headache types, diagnostic criteria and
the role of cervical procedural interventions in manage-
ment are widely debated. Purely clinical diagnostic criteria
for cervicogenic headache include unilateral pain, reduced
range of neck movement, ipsilateral shoulder and arm
discomfort, and mechanical precipitation of attacks by
awkward neck positions or external pressure against
occipital structures [5]. These criteria, however, have poor
interrater reliability and specificity [6,7]. Others argue that
in order to attain validity, a cervical source of the pain must
be identified via diagnostic blocks [1]. Reflecting this dis-
agreement, the International Headache Society (IHS) cri-
teria include evidence of causation via multiple different
modalities, including both clinical maneuvers and diag-
nostic blockade (Table 1C). This creates a certain tension
between definitional criteria that include response to
therapy and the prospect of performing invasive diagnos-
tic interventions in patients who likely do not have
cervicogenic headache, particularly as neck pain is a
prominent feature of migraine in over 73% of cases [8],
474
and as such neck injections are usually not warranted.
The extent of the diagnostic morass is highlighted in
the IHS definition, in which clinical diagnostic tests
“must have demonstrated reliability and validity. The future
task is the identification of such reliable and valid opera-
tional tasks.” Moreover, the clinical overlap between
cervicogenic headache and other primary headache syn-
dromes further complicates the criteria for the diagnosis of
cervicogenic headache.
We present a case of cervicogenic headache with trigemi-
nal distribution of pain and facial swelling that was fully—
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albeit not permanently—relieved by radiofrequency
lesioning of the TON at the C2–C3 facet joint. This serves
as proof of principle that referred CN V distribution pain
and even associated autonomic features can be amelio-
rated by disruption of the appropriate nociceptive cervical
pain afferents relayed via the spinal trigeminocervical
complex. A unique feature of this case was the significant
associated facial swelling, which we postulate was due
to trigeminal nerve-mediated neurogenic inflammation.
Given the clinical similarities seen in this case between
cervicogenic headache and trigeminal autonomic
cephalgias (TACs), we discuss the role of unified diagnos-
tic criteria to differentiate cervicogenic headache from
overlap syndromes with migraine and TACs, as well as the
use of cervical radiofrequency ablation in other primary
headache syndromes. Finally, we advocate for the supe-
riority of dedicated TON lesioning over the C3 medial
branch lesioning.
Case
A 38-year-old right-handed woman presented with 3 years
of right-sided facial and neck pain since a motor vehicle
accident with whiplash injury. The pain was cyclical, with
several months of severe pain followed by months of
relatively lessened pain. At its worst, the pain would keep
her from working as a respiratory therapist. The pain was
described as a burning, pressure-like sensation located in
the right neck, ear, jaw, eye, and right nostril, with allodynia
and burning sensation provoked by wind or hair touching
her on the right face and occasionally with breathing in the
right nostril. Associated with the pain exacerbations, she
experienced right facial swelling, erythema, and right eye
tearing; she did not report eye drooping. The pain was
increased by head rotation, Valsalva, coughing, sneezing,
and swallowing. The pain was not relieved by
carbamazepine, amitriptyline, cyclobenzaprine, metax-
alone, or topical lidocaine. The combination of gabapentin
and hydrocodone/acetaminophen provided limited benefit.
Past medical history included well-controlled migraines
characterized by throbbing pain in either temple with
associated phonophobia, photophobia, and nausea
lasting a few hours, occurring a few times a year, and
relieved by over-the-counter medications. Thus, the new
side-locked headache and associated symptoms funda-
mentally differed from those associated with her
prior migraines. Her medical history was also notable
for a congenital tracheoesophageal fistula status post tho-

racotomy, with presumed recurrent laryngeal nerve
lesion resulting in chronic left vocal cord paralysis and
mild hoarseness.
Her physical examination was notable for facial asymme-
try, with right-sided predominantly periorbital and man-
dibular facial swelling, but symmetric facial movements.
Extraocular movements, sensation to all modalities, and
hearing were intact. Speech was chronically hoarse, but
fluent, with no lingual, guttural, or buccal dysarthria. The
tongue and palate moved in the midline. There was no
change in taste. Gag was chronically absent. Shoulder
shrug and head turn strength were full. There was no
pronator drift. Deep tendon reflexes were brisk and sym-
metric, and Babinski response was absent bilaterally.
There was no ataxia, and station and gait were normal.
Spurling’s test was normal; however, there was marked
pain with palpation in the region of the upper cervical
facets on the right. There was no restriction of neck range
of motion, although palpation of the upper right cervical
facets produced pain radiating to the right arm and
occiput. Head magnetic resonance imaging (MRI) and
magnetic resonance angiogram were unremarkable.
Based on the focal unilateral facet tenderness, it was felt
that she had a combination of cervical nerve and trigemi-
nal involvement due to a presumed cervicogenic head-
ache. She first underwent diagnostic medial branch
blocks with 0.5 mL of 1% lidocaine at the right C3, C4,
and C5 levels to determine if facet arthropathy at any of
these levels was acting as a primary pain generator.
These blocks resulted in 90% relief of her right cervical
and occipital pain that lasted for several hours, the
expected duration of the local anesthetic. To confirm effi-
cacy, the same diagnostic blocks were repeated a week
later, again with 90% relief in her right cervical and
occipital pain. Based on the positive diagnostic blocks, it
was felt that she likely did have cervicogenic pain origi-
nating in part from facet disease, and that she might
benefit from cervical medial branch radiofrequency
lesioning. The impedance was between 300 and 800
ohms. Sensory stimulation at 50 Hz and motor stimula-
tion at 2 Hz were carried out prior to each cycle of
lesioning, which elicited discomfort but no motor stimu-
lation. Denervation was performed for 60 seconds at
80°C with single lesions adjacent to the C3, C4, and C5
articular processes; she had marked but only temporary
improvement of her pain and right facial swelling. Repeat
MRI with and without contrast with thin cuts through the
skull base to look at the jugular foramen was normal, as
was MRI of the anterior neck. Cervical spinal MRI
showed minimal degenerative changes. She underwent
a second radiofrequency lesioning of the right C3, C4,
and C5 medial branches a year after her initial proce-
dure, with 50% improvement in her right-sided pain and
swelling. The pain returned after 5 months, and she had
a third right C3, C4, and C5 medial branch
radiofrequency lesioning at that time, which provided no
relief. As it was felt that she might still have cervicogenic
pain involving the TON, she underwent a diagnostic right
TON block with 0.5 mL of 1% lidocaine over the C2 and
Autonomic Features in Cervicogenic Headache
C3 facet pillars with excellent pain relief, which was con-
firmed on repetition a week later. She proceeded to
radiofrequency lesioning of the right TON via multiple [3]
focal lesionings, again for 60 seconds at 80°C, at and
just inferior to the border of the C2 and C3 facet pillars.
Following the procedure, she had complete resolution of
her symptoms, including her auricular, ocular, and nasal
pain, as well as her right facial pain and swelling, and
she was able to titrate off of gabapentin (2,400 mg/d)
and hydrocodone/acetaminophen (5 mg/500 mg Q6
hours) and return to work. This improvement lasted a
year and a half, before her symptoms returned, and she
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had repeat right C2–C3 TON radiofrequency lesioning,
again with abolition of her pain, facial swelling, tearing,
and injection.
Discussion
Here, we discuss a patient with cervicogenic headache
relieved by cervical blocks and ultimately radiofrequency
ablation. There are a number of unique features of this
case. The headache syndrome was accompanied by
autonomic features, which were also relieved by both local
anesthetic blockade and radiofrequency neurolysis. The
overlap between cervicogenic headache and the TACs
seen in this case highlights several issues: the complexity
of appropriate and useful diagnostic criteria for
cervicogenic headache, the role of cervical injection for
cervicogenic headache, and the potential overlap syn-
dromes with TAC and migraine. Lastly, the greater efficacy
of TON lesioning over the C3 medial branch lesioning
observed in this patient despite the fact that the TON
arises from the C3 medial branch highlights the impor-
tance of careful selection of interventions and potentially
the effects of anatomic variability among individuals.
Another notable aspect of this case was the patient’s
profound periorbital and mandibular swelling, and its relief
by cervical medial branch blockade and lesioning. Ipsilat-
eral eyelid edema has been described in early literature on
cervicogenic headache [9]. In the Cervicogenic Headache
International Study Group criteria, it falls under category
VI, rarely occurring associated phenomena, and is specifi-
cally noted to be present all the time, not only during
attacks as the described patient experienced [5]. In TACs,
periorbital edema is relatively common, and hypotheses to
explain this phenomenon have included trigeminal dis-
charge [10], central autonomic dysregulation, and para-
sympathetic hyperactivity associated with hypothalamic
disturbance [11], as well as compression of pericarotid
sympathetic fibers due to perivascular edema from para-
sympathetic overactivity [12]. While the TACs are felt to
originate in the hypothalamic–pituitary axis [13,14], the
spinal trigeminocervical complex implicated in cervico-
genic headache would seem less likely to cause direct
hypothalamic disturbance or pericarotid parasympathetic
overactivity. The convergence of spinal and trigeminal
afferents in the spinal trigeminocervical complex may also
indirectly activate the superior salivatory nucleus mediat-
ing parasympathetic activity [15] as experimental stimula-
tion of the greater occipital nerve branch of C2 has
475
Giblin et al.
resulted in ipsilateral tearing, ptosis, and conjunctival
injection in rats [16]; however, the potential anatomical
connections for these effects are less clear. Alternatively,
the trigeminal-distribution edema seen in cervicogenic
headache could be due to neurogenic inflammation,
whereby the stimulation of primary trigeminal nociceptive
central terminals causes antidromic propagation in the
trigeminal first-order nociceptors, peripheral release of
neuropeptides calcitonin gene-related peptide and sub-
stance P, and subsequent vasodilation and increased
capillary permeability [17,18]. However, such a mecha-
nism would also need to explain the activation of the
primary central trigeminal nociceptive terminals sufficient
to generate the neurogenic inflammation. We theorize that
in cervicogenic headache, the first-order trigeminal noci-
ceptive neuron may be stimulated by nitric oxide from
either the postsynaptic trigeminocervical complex neuron
via retrograde synaptic transmission [19], or from the par-
allel occipital neuron activated by cervical pathology [20].
Such a mechanism, based on the production of postsyn-
aptic or perisynaptic nitric oxide, and the development of
neurogenic inflammation in the presynaptic trigeminal
neuron, would require in vitro validation.
Although periorbital edema has been documented in
cervicogenic headache, the potential clinical overlap in
this case with the TACs illustrates the difficulty of diagnosis
of cervicogenic headache. Significant overlap also exists
in the symptomatology of cervicogenic headache,
migraine, and hemicrania continua (HC). Per Sjaastad
et al., 20% of cervicogenic headache is associated with
photophobia and other features that are classically
thought of as “migrainous,” including phonophobia,
nausea, dizziness, and ipsilateral blurred vision, although
“to a lesser degree” than in migraine [5]. Further compli-
cating matters, neck pain is strikingly prevalent in
migraineurs: in a study of 113 migraineurs who had been
examined by headache specialists and felt to have pure
migraine, neck pain was actually more prevalent in
migraine than nausea, with up to 73% of migraines occur-
ring with concomitant neck pain [8]. Studies have found
increased neck muscle girth in migraineurs [21], as well as
increased antagonist muscle activity on electromyogram
during neck movements [22]. Adding to the complexity,
orbital, facial, and auricular swelling has been reported in
HC [23], which can be primary or posttraumatic [24].
Moreover, an overlap syndrome of cervicogenic headache
and HC has been reported [25].
While the pathophysiology of cervicogenic headache is
relatively well established, the clinical entity of cervicogenic
headache is strikingly convoluted. There are multiple sets
of diagnostic criteria as well as differing opinions about the
role of interventional approaches in diagnosis and treat-
ment. As noted above, the clinical criteria for cervicogenic
headache suffer from poor interrater reliability and speci-
ficity with regard to range of motion and precipitation by
external pressure [6]. On the interventional end of the
diagnostic spectrum, the IHS criteria for the diagnosis of
cervicogenic headache include abolition of pain via block-
ade of nerves that innervate responsible cervical lesions.
476
Certainly, performing cervical medial branch blocks on
large populations of refractory migraineurs with neck pain
is inappropriate. Given reported magnitude of the placebo
effect in interventional pain studies, assessing non-
placebo benefits of cervical and occipital procedures is
particularly challenging. Nonetheless, there is evidence
that suboccipital steroid injection in the area of the greater
occipital nerve may reduce the frequency of cluster head-
ache [26,27], and greater occipital nerve blocks may be
efficacious for short-lasting unilateral neuralgiform head-
ache with conjunctival injection and tearing (SUNCT syn-
drome) [28], HC [29], and migraine [30]. Occipital nerve
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stimulation is being investigated for a number of primary
headache syndromes [31].
These findings raise the question of whether cervical
pathology may contribute to these other headache types
and whether interruption of cervical somatosensory input
may provide benefit in the absence of cervical pathology.
Thus, potential analgesic response from medial branch
and TON blockade in non-cervicogenic primary headache
syndromes may confound the specificity of cervical facet
blocks in diagnosing cervicogenic headache.
While the described patient had a history of cervical whip-
lash injury and a physical exam finding of precipitation of
pain with palpation of right cervical facets, both consistent
with a clinical diagnosis of cervicogenic headache, she
had less therapeutic benefit from C3, C4, and C5 medial
branch lesioning than from TON lesioning. This empha-
sizes the importance of appropriate choice of level of
cervical medial branch lesioning in the treatment of
headache. This is concordant with the findings of Govind
and colleagues that more aggressive lesioning was
required for TON block compared with earlier studies of
lower cervical medial branch radiofrequency ablation
[32,33]. While six passes in third occipital lesioning (as
performed in Govind et al.) may not be well tolerated in all
patients with only local anesthetic and without monitored
anesthesia care, it may be that dedicated TON
radiofrequency ablation using a smaller number of lesions
can suffice.
In conclusion, despite having well-defined anatomic
pathophysiology, the diagnosis and treatment of
cervicogenic headache present a clinical conundrum.
There is significant overlap with the TACs and migraine,
which can hinder clinical diagnosis. Interventional diagno-
sis may be confounded by differences in technique and by
benefit from intervention in primary headache syndromes
other than cervicogenic headache. This case documents
that trigeminal pain can be a component of cervicogenic
headache, and that it can be relieved by cervical medial
branch and TON neurolysis. The case also represents a
unique proof of principle in that not only CN V pain but also
presumed neurogenic inflammation in a CN V distribution
can be relieved by blockade of cervical nociceptive inputs.
Finally, multiple components of cervicogenic headache,
TACs, and migraine may be present in individual patients,
thus underscoring the importance of future investigation
into shared mechanisms of headache pathogenesis.

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