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CLINICAL REPORT
Unsuccessful Pulsed Radiofrequency of the
Sphenopalatine Ganglion in Patients with
Chronic Cluster Headache and Subsequent
Successful Thermocoagulation
Damian Claudio Bendersky, MD; Santiago Matias Hem, MD; Claudio Gustavo
Yampolsky, MD
Department of Neurosurgery, Hospital Italiano de Buenos Aires, Buenos Aires, Argentina
& Abstract: We present the results of pulsed and continuous radiofrequency (CRF) of the sphenopalatine ganglion in a
case series of 3 patients with chronic cluster headache (CCH).
Three patients were referred to our neurosurgical department because of CCH, which was refractory to pharmacological treatment. They underwent pulsed radiofrequency of the
sphenopalatine ganglion (PRF-SPG), and the procedure was
performed through an infrazygomatic approach. In the PRF
procedures, we applied 2 cycles of PRF at 42°C and 45 V for
120 seconds, with a pulse frequency of 2 Hz and a pulse
width of 20 ms. In those procedures where thermocoagulation was carried out, 2 CRF lesions at 80°C for 90 seconds each
were performed. Following corticosteroid and local anesthetic (40 mg of methylprednisolone and 1 mL of 1% lidocaine) injection, 2 patients had no pain relief at all, whereas
the third one experienced a partial response, which lasted
only 1 month and his pain then returned to its baseline level.
Thus, this outcome was assessed as a nonsustained partial
response. Therefore, all of them underwent a CRF lesioning
of the SPG, and after this procedure, they achieved complete
pain relief until the end of the follow-up period. Further-
n Claudio
Address correspondence and reprint requests to: Damia
noma de Buenos
Bendersky, MD, Juan Domingo Peron 4190, Ciudad Auto
Aires C1181ACH, Argentina. E-mail: [email protected].
Submitted: August 11, 2014; Revised: December 7, 2014;
Revision accepted: December 9, 2014
DOI. 10.1111/papr.12288
© 2015 World Institute of Pain, 1530-7085/15/$15.00
Pain Practice, Volume 15, Issue 5, 2015 E40–E45
more, the associated autonomic manifestations disappeared.
The 3 patients presented in this case series failed to achieve
adequate pain relief after PRF-SPG. However, these same
patients subsequently underwent a successful CRF of the
SPG. &
Key Words: cluster headache, sphenopalatine ganglion,
pulsed radiofrequency, continuous radiofrequency, thermocoagulation
INTRODUCTION
Cluster headache (CH) is a trigeminal autonomic cephalalgia, a condition that is characterized by severe unilateral
headache and cranial parasympathetic manifestations.1–9
Approximately 10% to 15% of patients develop chronic
cluster headache (CCH).6,7,10,11 Although its treatment is
essentially pharmacological, involving both prophylactic
and acute measures, up to 15% to 20% of patients do not
respond adequately to conservative management. In these
cases, as well as those in which the side effects of the
medications are intolerable a sphenopalatine ganglion
(SPG) block may be indicated. Although several methods
for blockade are proposed in the literature, we previously
used continuous radiofrequency (CRF) of the SPG in
patients with medically refractory CCH.2,5–8,10–13 However, there may be some complications following this
procedure, such as hyperpathia or deafferentation pain in
PRF of the Sphenopalatine Ganglion E41
theterritoryofthemaxillarybranchofthetrigeminalnerve;
permanent or transient hypesthesia; hypersensitivity or
dysesthesia in the palate; maxilla;, gums; cheek or posterior
pharynx; in addition to dryness of the eye and reflex
bradycardia during radiofrequency lesioning.2–4,7,10,11,14
Thus, we decided to try pulsed radiofrequency (PRF), a
nondestructive method which was found to be effective in
other studies for this and other pain conditions, to avoid
complications due to neural tissue damage.3,4,11,14,15
We present a case series of 3 patients with CCH who
underwent pulsed radiofrequency of the sphenopalatine
ganglion (PRF-SPG) without obtaining adequate pain
relief. Finally, these patients achieved complete pain
relief following CRF plus SPG block.
CASE SERIES
Between January and May 2013, 3 patients were
referred to our neurosurgical department because of
unbearable headache. All of them fulfilled the diagnostic
criteria of the International Headache Society (IHS) for
CH (Table 1). The subjects were evaluated and treated
by a neurologist who specialized in headaches. These
patients tried several pharmacological treatments before
being referred to our department, but the results were
poor. The 3 patients suffered from CCH, as their
headache presented remission periods, which lasted
< 1 month, or they did not have remission periods,
depending on each case.1 After giving written consent
for the procedure, they underwent PRF-SPG without a
previous diagnostic block of this ganglion. The intensity
and frequency of the pain attacks were measured before
and after the procedure. The former variable was
evaluated with the visual analog scale (VAS). We
Table 1. Diagnostic criteria of the International Headache Society for cluster headache (ICHD-3)1
A. At least 5 attacks fulfilling criteria B to D
B. Severe or very severe unilateral orbital, supraorbital, and/or temporal
pain lasting 15 to 180 minutes (when untreated)
C. Either or both of the following:
At least one of the following symptoms or signs, ipsilateral to the
headache:
Conjunctival injection and/or lacrimation
Nasal congestion and/or rhinorrhoea
Eyelid edema
Forehead and facial sweating
Forehead and facial flushing
Sensation of fullness in the ear
Miosis and/or ptosis
A sense of restlessness or agitation
D. Attacks have a frequency between one every other day and 8 per day for
more than half of the time when the disorder is active
E. Not better accounted for by another ICHD-3 diagnosis
assessed the outcome of the procedure as follows:
complete response (complete pain relief); partial
response (≥ 50% reduction of intensity and frequency
of the pain attacks); and poor response (not reaching the
criteria for partial response or no pain relief at all). In
case of pain relapse, we would have repeated the PRFSPG if there was a sustained complete or partial
response following the first procedure. However, we
would have performed a CRF lesioning of the SPG in the
event of a poor response.
Procedural Technique
The procedure was performed through an infrazygomatic approach, as described in the literature.2–4,7,10,11,13–
17
It is carried out under fluoroscopic guidance, with the
patient in supine position. The pterygopalatine fissure is
visualized with lateral fluoroscopy. Although the needle
may also be inserted anterior to the mandible, we use a
point in the coronoid notch just below the inferior edge
of the zygomatic arch as the entry point. Following
subcutaneous injection of 2 mL of 1% lidocaine, a 20-g,
10-cm needle with 5-mm active tip is introduced using
lateral fluoroscopy. It must be noted that the usage of a
curved cannula may facilitate the procedure. The needle
tip must be located within the pterygopalatine fossa, just
lateral to the nasal wall. Next, an anteroposterior view is
obtained to check the needle position, which should be
at the level of the middle turbinate. If it is properly
placed, we can pass to the next step, or else we must
correct its position. Then, its location is neurophysiologically verified by sensory stimulation at 50 Hz.
Paresthesia should be elicited at the roof of the nose. If
paresthesia is felt in the upper teeth, cheek, and/or upper
lip, the electrode is stimulating the maxillary nerve or its
branches and the needle must be repositioned caudally
and medially. If paresthesia is present in the hard palate,
the greater and lesser palatine nerves are being stimulated and thus, the tip of the electrode must be moved
posteriorly, medially, and superiorly.10,11,13,17 When
the surgeon believes that the cannula is in the target, PRF
or CRF is performed. In PRF procedures, we applied 2
cycles of PRF at 42°C and 45 V for 120 seconds, with a
pulse frequency of 2 Hz and a pulse width of 20 ms. In
those procedures in which thermocoagulation was
carried out, 2 CRF lesions at 80°C for 90 seconds each
were performed. Corticosteroid and local anesthetic
(40 mg of methylprednisolone and 1 mL of 1% lidocaine) injection within the pterygopalatine fossa was
carried out only when CRF was used.
E42 BENDERSKY ET AL.
RESULTS
The demographic variables and pain characteristics of
the 3 patients are shown in Table 2. Following PRF-SPG,
2 patients had no pain relief at all, whereas the third one
experienced a partial response, which lasted only
1 month. His pain then returned to its baseline level.
Thus, this outcome was assessed as a nonsustained
partial response. Therefore, all patients underwent a CRF
lesioning of the SPG. After this procedure, they achieved
complete pain relief until the end of the follow-up period.
Furthermore, the associated autonomic manifestations
disappeared. There were no complications in this case
series, including PRF and CRF procedures.
The first patient was a 53-year-old woman who started
with right episodic CH 15 years before being referred to
our department. She was initially treated with verapamil
as prophylaxis, while sumatriptan and oxygen inhalation
were used for acute episodes. Nine years after the
diagnosis, her episodic headache evolved to CCH. She
had remission periods, which lasted < 1 month. Other
drugs were tried (ergotamine and topiramate) but had
little to no effect. Finally, she was referred to us
14 months ago. She underwent right PRF-SPG without
response. Three months later, the patient accepted to
undergo a CRF of the SPG and following the thermoco-
agulation, she achieved complete pain relief until the end
of the 11-month follow-up period. Currently, she
remains on verapamil for prophylactic therapy.
The second patient was a 37-year-old woman with
right CCH since age 33. Her headache arose de novo
and was associated with several autonomic signs and
symptoms. She never had remission periods. At the
beginning, verapamil was used for prophylactic treatment. It was useful for < 2 years, when the headache
became refractory to pharmacological treatment despite
using not only first-tier drugs, but also second-tier ones:
lithium, topiramate, carbamazepine, pregabalin, and
amitriptyline. First, she had good response to corticosteroids, but then her pain became unresponsive to it.
Given her refractory pain, right PRF-SPG was carried
out, but she did not achieve any pain relief. Four months
following this first procedure, CRF of the same ganglion
was performed. Thereafter, she has suffered no headache for the next 8 months. She is receiving only
topiramate for prophylaxis.
The last patient was a 36-year-old man who started
with left CCH 7 years before the PRF-SPG. He did not
present remission periods, and his major complaints
were pain as well as eyelid edema and lacrimation.
All prophylactic drugs used (i.e., verapamil, lithium,
Table 2. Demographic variables and pain characteristics
Patient 1
Patient 2
Patient 3
Age
Gender
Location of pain
Type of cluster headache
Associated autonomic manifestations
53
Female
Supraorbital/temporal
Chronic
Conjunctival injection, lacrimation,
nasal congestion, and rhinorrhoea
Mechanical allodynia
Average frequency of
attacks (before PRF-SPG)
Intensity (VAS) of pain
during the attacks (before PRF-SPG)
Duration of each
attack (before PRF-SPG)
Average frequency
of attacks (1 week after PRF-SPG)
Intensity (VAS) of pain during
the attacks (1 week after PRF-SPG)
Duration of each attack
(1 week after PRF-SPG)
Response to PRF-SPG
Associated autonomic
manifestations
(1 week after PRF-SPG)
Response to CRF of the SPG
Associated autonomic
manifestations after CRF of the SPG
Present
3/day
37
Female
Orbital/supraorbital
Chronic
Conjunctival injection, lacrimation,
nasal congestion, rhinorrhoea,
facial sweating, and ptosis (mild)
Present
4/day
36
Male
Orbital/supraorbital/temporal
Chronic
Eyelid edema, lacrimation,
conjunctival injection, nasal
congestion, and rhinorrhoea
Present
4/day
10
10
10
2 to 3 hours
1 to 2 hours
2 to 3 hours
3/day
4/day
1/day
10
10
5
2 to 3 hours
1 to 2 hours
2 to 3 hours
Poor
No improvement
Poor
No improvement
Partial (nonsustained)
Partial improvement
Complete
Disappeared
Complete
Disappeared
Complete
Disappeared
CRF, continuous radiofrequency; PRF, pulsed radiofrequency; PRF-SPG, pulsed radiofrequency of the sphenopalatine ganglion; VAS, visual analog scale.
PRF of the Sphenopalatine Ganglion E43
topiramate) were ineffective, and he needed abortive
treatment of the acute attacks very frequently. The
patient developed depression during the course of his
treatment with topiramate. The topiramate was suspended and verapamil was restarted, since the former
was unhelpful and depression is a known adverse effect
of this drug. Verapamil failed again and thus, lithium
was tried. He achieved minimal results with this therapy,
and therefore, PRF-SPG was carried out 1 year ago.
Following the intervention, he experienced a marked
reduction of both intensity and frequency of the pain
attacks; nevertheless, the associated autonomic manifestations diminished, but they were still present. Unfortunately, this partial response lasted only 1 month. Six
weeks after the relapse, the patient was desperate for a
long-term solution. At last, he underwent CRF of the
SPG and since then, he had no pain attacks, despite not
using prophylactic treatment currently. Almost
10 months later, he is still asymptomatic.
changes.18 It is important since the pain of CH is
thought to be due to activation of the ophthalmic nerve.8
CH, as well as the other identified trigeminal autonomic
cephalalgias, involves the activation of the trigeminal
autonomic reflex, whose afferent limb is the trigeminal
nerve and the efferent one is represented by the
parasympathetic fibers of the greater superficial petrosal
nerve.9,20 One hypothesis about its physiopathology is
that efferent parasympathetic outflow from the SPG
may both initiate autonomic manifestations and activate
trigeminovascular sensory afferents, which in turn may
initiate the pain.18 The increased parasympathetic outflow may be originated centrally because of a hypothalamic disturbance, with likely involvement of a
trigemino-hypothalamic pathway. Also, descending
fibers from the hypothalamus to the trigeminal nucleus
caudalis could trigger the pain.6,8,19
As mentioned previously, there may be some complications following CRF of the SPG. Almost all of
DISCUSSION
The SPG is located within the pterygopalatine fossa, just
below the maxillary nerve. Despite being a parasympathetic ganglion, it also receives sensory, motor, and
sympathetic roots (Figure 1). These connections of the
SPG, as well as its anatomical location, may help in
understanding the physiopathology of the CH and the
complications following the ablation of this ganglion.
Even though the physiopathology of CH is still
unknown, the hypothalamus is thought to be the
generator of this disease because of its circadian and
circannual periodicity and the activation of the posterior
hypothalamus found in neuroimaging studies that were
undertaken during the attacks. Furthermore, activation
of the parasympathetic outflow from the superior salivary nucleus via the SPG is supposed, explaining the
autonomic manifestations of CH and the likely role of
the SPG at least in this aspect of the disease.4–6,8–11,18,19
Indeed, it was shown that low frequency (5 Hz) SPG
stimulation could induce cluster-like attacks with autonomic features. According to the explanation of the
authors, this induction may be due to the release of
neurotransmitters from parasympathetic efferents,
which activate or at least modulate trigeminal nociceptors. On the other hand, high frequency (80 to 120 Hz)
SPG stimulation may activate sensory fibers from the
maxillary nerve, which converge in the trigeminal
nucleus caudalis with afferents from the ophthalmic
branch, leading to antinociceptive modulatory
Figure 1. The parasympathetic root has its origin in the superior
salivary nucleus (SSN), and these preganglionic axons pass
through several neural structures before reaching the SPG:
nervus intermedius (or nerve of Wrisberg) (NI), facial nerve (FN),
geniculate ganglion (GG), greater superficial petrosal nerve
(GSPN), and vidian nerve (VN). The parasympathetic fibers
synapse in the SPG, and the postganglionic fibers innervate the
nasal cavity, the mucosa of the palate, the nasopharynx, and the
lacrimal gland. The sympathetic root is formed by postganglionic
fibers from the superior cervical ganglion (SCG), which travel
through the internal carotid plexus (ICP), the deep petrosal nerve
(DPN) and the VN before entering the SPG. These axons do not
synapse in the SPG, and they are distributed to the nasal cavity
and pharynx. The sensory root comes from the maxillary nerve,
and its fibers innervate the nose, throat, and sinuses. The motor
root seems to be derived from the NI, and it may actually be a
bundle of sympathetic fibers which arise in the brainstem.2,3,11,14,20
E44 BENDERSKY ET AL.
them can be explained by its close proximity with the
maxillary nerve and its branches. Indeed, hypesthesia of
the palate may be seen as a predictable consequence of
CRF of the SPG.3,4,10,11,14 Sanders and Zuurmond
reported that maxillary hyperpathia was the major
complication in 6.1% of 66 patients treated with CRF
of this ganglion.10 The rationale for using PRF-SPG is
to avoid these complications, as PRF, unlike CRF, is
thought to produce its effects by creating high intensity
electric fields without generating relevant thermal
injury of the neural tissue surrounding the tip of the
electrode. The tissue temperature rise using a certain
voltage is much less for PRF than for CRF because the
pulse duration is only a small percentage of the time
between pulses. Thus, CRF is used for tissue destruction, whereas PRF would be useful for those cases in
which CRF may produce complications or side effects
due to thermal injury.3,4,10,14,21–23 The authors believe
that both an accurate needle placement and the usage
of electrical stimulation during the procedure are
essential to decrease the occurrence of complications
of CRF.
We found only 3 articles in which PRF-SPG was used,
and all of them achieved good results following the
procedure. However, these studies included other types
of facial pain than CCH.4,14,15 In the article of Bayer
et al., only 27% of 30 patients were diagnosed with SPG
neuralgia (entity that is now classified as CH by the
IHS), while atypical facial pain was the most frequent
etiology. All patients had a previous positive response to
a diagnostic block of the SPG. After PRF-SPG, 14%
reported no pain relief, whereas 21% and 65% had
complete and mild-to-moderate pain relief, respectively.14 Chua et al. presented 2 patients with CCH
and 1 patient with episodic CH who underwent PRFSPG. There was a complete response in 2 of them and a
partial response in the other one. Nevertheless, the
follow-up period was quite short, lasting only
4 months.4 Shah and Racz reported a case in which
PRF-SPG was used to treat post-traumatic headache.
Following the intervention, this patient obtained longterm pain relief.15
There are several topics that should be discussed.
First, we believe that the major limitation of our case
series is the small number of patients; furthermore,
this is a retrospective study. Second, all of our
patients had CCH, which is thought to have worse
results after CRF of the SPG than episodic CH.7,10 In
fact, Sanders and Zuurmond reported that 60.7% of
56 patients with episodic CH and 30% of 10 patients
suffering from CCH achieved complete pain relief
following CRF. Because of the small number of
patient with CCH in their study, the authors concluded that CRF of the SPG is effective only for
episodic CH.10 Third, regarding PRF parameters, we
used the same as those of Bayer et al.14 We used the
above mentioned parameters because they were
effective in the previous case series, and we have
used these parameters for PRF of the dorsal root
ganglion. Chua et al. (4 Hz, 42°C, 10 ms, 45 V,
6 minutes), as well as Shah and Racz (2 Hz, 42°C,
20 ms, 6 minutes), used other settings.4,15 We cannot
rule out that other PRF parameters may be more
effective than those utilized in this study. Fourth, all
patients in our series had mechanical allodynia, which
may be associated with reduced response to treatment, although it was not demonstrated for CH.4,24
In the study of Chua et al.,4 the only patient who had
allodynia experienced less pain relief than the other 2.
Fifth, we cannot conclude if the success of the last
procedure was due to the CRF of the SPG, the
corticosteroid injection within the pterygopalatine
fossa, or a combination of both treatments. For
example, Sanders and Zuurmond achieved good
results after CRF without performing corticosteroid
injection in the SPG, whereas Pe~
narrocha-Diago also
reported favorable results following SPG corticosteroid injection alone.5,10 Other authors, as we did in
this article, carry out both treatments during the same
procedure.7,11 However, anesthetic blockade, plus
corticosteroid injection, seems to produce only temporary improvement.2,3,5,25 Sixth, we must comment
that the only patient who achieved some improvement in autonomic manifestations also experienced at
least some pain relief following PRF-SPG. Furthermore, all patients were free of autonomic manifestations after CRF of the SPG. It could be related to the
interruption of the parasympathetic fibers in the SPG.
It also shows the relationship between pain and
parasympathetic manifestations.
SUMMARY
The 3 patients presented in this case series failed to
achieve adequate pain relief after PRF-SPG. However,
these same patients subsequently underwent a successful
CRF of the SPG. Thus, we will continue to perform CRF
of this ganglion for CCH patients until the availability of
higher level evidence of the efficacy of PRF-SPG in this
population.
PRF of the Sphenopalatine Ganglion E45
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