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Monday, February 5, 2018

New Studies Point To Common Etiologic Cause of Migraines and Essential Hypertension? Sphenopalatine Ganglion (SPG) has a Central Role.

This post was originally published on SphenoPalatineGanglionBlocks.com

Two new  studies  published Jan 1, 2018  in the International Journal of Cardiology and Cephalgia point the way for a new understanding in the cause of Migraines and Hypertension being closely linked.  This may open the doors to new ways to examine the underlying causes of two common disorders.

The PUBMED abstracts of all studies cited are available  at the bottom of this post.
The article in Cephalgia , “Migraine and the Risk of Incident Hypertension Among Women” was a prospective cohort study of 29,040 women without hypertension at baseline.  The study examined the increase risk of hypertension in women   “classified as having active migraine with aura, active migraine without aura, a past history of migraine, or no history of migraine”  The article concluded “Women with migraine have a higher relative risk of developing hypertension compared to women without migraine.”
The second article,”Bilateral sphenopalatine ganglion block reduces blood pressure in never treated patients with essential hypertension.  A randomized controlled single-blinded study  in the International Journal of Cardiology.
Findings of decreased  24 hour and daytime blood pressure decreased in the study group a month after SPG block.  Significant response was noted in 36% of ptients identified as responders.  The study concluded that “SPG block is a promising, minimally invasive option of BP decrease in hypertensives”
 Combining these two studies and understanding the complex natures of the Sphenopalatine Ganglion with its Sympathetic and Parasympathetic fibers ties together autonomic nervous system that traverses the the trigeminal nerves along with the somatosensory trigeminal fibers.
Increasing the frequency of SPG Blocks increase their effectiveness.  Self-Administration will ultimately make all of these interventions far more effective and affordable.
A third study in the Journal of Headache Pain that was published on January 18, 2018  looked at Sphenopalatine Ganglion Stimulation as a treatment for Cluster Headache.  Cluster Headache is one of the Autonomic Trigeminal Cephalgias that also is controlled by the Trigeminal Nerve, both the Somatosensory nerves and the Sympathetic and Parasympathetic nerves of the autonomic nervous system.
The study “Sphenopalatine ganglion stimulation for Cluster Headaches, results from a large, open-label European registry.  The study concluded that “SPG stimulation is an effective therapy for CH patients providing therapeutic benefits and improvements in use of medication as well as headache impact and quality of life.”
Another article, Diagnosis, pathophysiology and management of cluster headache.” published inLancet Neurology on January 17, 2018  The study states “Cluster headache is now thought to involve a synchronised abnormal activity in the hypothalamus, the trigeminovascular system, and the autonomic nervous system. ”  These are the exact nervous systems structures discussed in the previous articles.
Cluster headaches are “trigeminal autonomic cephalalgia characterised by extremely painful, strictly unilateral, short-lasting headache attacks accompanied by ipsilateral autonomic symptoms or the sense of restlessness and agitation, or both”  The articl describes CH  Cluster headachehypothesized to  “involve a synchronised abnormal activity in the hypothalamus, the trigeminovascular system, and the autonomic nervous system.”
These same structure are also of great interest to doctors treating orofacial pain and TMJ disorders.  Shimshak in his 1998 paper showed that patients with TMJ disorders utilized health care 300% the rate of non-TMJD in every singe field of medicine (except pregnancy and childbirth).  It has been reported (not confirmed) that Blue Cross of Pennsylvania whose data was used for the studies made Dr Shimshak destroy research papers related to the study. ( I presume this was due to not wanting to cover TMJ disorders”.  This is understandable when one considers that the exact same nervous structures are invloved in TMJ disorders ie the Somatosensory nerves of the trigeminal nervous system along with Sympathetic and Parasympathetic fibers of the autonomic nervous system that travel along the trigeminal branches.
Neuromuscular Dentistry has been extremely effective at treating not just TMJ disorders but also Migraines, Chronic Daily Headaches, Sinus Pain Eye pain , trigeminal autonomic cephalgias and orofacial pain. Much of the success of Neuromuscular Dentistry may have to do with the actions of the Myomonitor (also BioTens) on both the somatosensory nerves of the trigeminal and facial nerve but also on the sympathetic and parasympathetic nerves of the autonomic nervous system that travel with the somatosensory nerves.
The Myomonitor would act on the Sphenopalatine ganglion (pterygopalatine ganglion) where it sits in the pterygopalatine fossa on the second division (maxillary) of the trigeminal nerves bilaterally.  It has a 50 year safety record of using skin electrodes to deliver ultra-low stimulation to the sphenopalatine ganglion.   This connection should be easy to see after reading the article on Sphenopalatine Ganglion Stimulation.

Cephalalgia. 2018 Jan 1:333102418756865. doi: 10.1177/0333102418756865. [Epub ahead of print]

Migraine and the risk of incident hypertension among women.


Background Few studies have examined whether migraine is associated with an increased risk of incident hypertension. Methods We performed a prospective cohort study among 29,040 women without hypertension at baseline. Women were classified as having active migraine with aura, active migraine without aura, a past history of migraine, or no history of migraine. Incident hypertension was defined as new physician diagnosis or newly self-reported systolic or diastolic blood pressure ≥140 mmHg or ≥90 mmHg respectively. Cox proportional hazards models were used to evaluate the association between migraine and incident hypertension. Results During a mean follow-up of 12.2 years, 15,176 incident hypertension cases occurred. Compared to those with no history of migraine, women who experience migraine with aura had a 9% increase in their risk of developing hypertension (95% CI: 1.02, 1.18); women who experience migraine without aura had a 21% increase in their risk of developing hypertension (95% CI: 1.14, 1.28); and women with a past history of migraine had a 15% increase in their risk of developing hypertension (95% CI: 1.07, 1.23). Conclusions Women with migraine have a higher relative risk of developing hypertension compared to women without migraine.


Migraine; epidemiology; hypertension; women
Int J Cardiol. 2018 Jan 1;250:233-239. doi: 10.1016/j.ijcard.2017.10.042. Epub 2017 Oct 16.

Bilateral sphenopalatine ganglion block reduces blood pressure in never treated patients with essential hypertension. A randomized controlled single-blinded study.



Sympathetic fibers connect sphenopalatine ganglion (SPG) with the central nervous system. We aimed to study the effect of SPG block in blood pressure (BP) in never treated patients with stage I-II essential hypertension.


We performed bilateral SPG block with lidocaine 2% in 33 hypertensive patients (mean age 48±12years, 24 men) and a sham operation with water for injection in 11 patients who served as the control group (mean age 51±12years, 8 men). All patients have been subjected to 24h ambulatory blood pressure monitoring prior and a month after the SBG block in order to estimate any differences in blood pressure parameters. We defined as responders to SBG block those patients with a 24h SBP decrease ≥5mmHg.


We found that 24h and daytime DBP (p=0.02) as well as daytime DBP load (p=0.03) were decreased in the study group a month after SPG block. In addition, a significant response was noted in 12/33 responders (36%) regarding: a. SBP and DBP during overall 24h and daytime (p<0 .001="" and="" b.="" bp="" c.="" daytime="" dbp="" differences="" early="" found="" group.="" in="" load.="" morning="" night-time="" no="" operation="" p="" periods="" pre-awake="" regarding="" sbp="" sham="" the="" were="">


SPG block is a promising, minimally invasive option of BP decrease in hypertensives, probably through SNS modulation. Additionally, due to its anesthetic effect, SPG block might act as a method of selection for those hypertensive patients with an activated SNS before any other invasive antihypertensive procedure.


24h blood pressure measurement (24h ABPM); Arterial hypertension; Neural block; Sphenopalatine ganglion
J Headache Pain. 2018 Jan 18;19(1):6. doi: 10.1186/s10194-017-0828-9.

Sphenopalatine ganglion stimulation for cluster headache, results from a large, open-label European registry.



Cluster headache (CH) is a disabling primary headache disorder characterized by severe periorbital pain. A subset of patients does not respond to established pharmacological therapy. This study examines outcomes of a cohort of mainly chronic CH patients treated with sphenopalatine ganglion (SPG) stimulation.


Patients were followed in an open-label prospective study for 12 months. Ninety-seven CH patients (88 chronic, 9 episodic) underwent trans-oral insertion of a microstimulator targeting the SPG. Patients recorded stimulation effect prospectively for individual attacks. Frequency, use of preventive and acute medications, headache impact (HIT-6) and quality of life measures (SF-36v2) were monitored at clinic visits. Per protocol, frequency responders experienced ≥ 50% reduction in attack frequency and acute responders treated ≥ 50% of attacks. HIT-6 responders experienced an improvement ≥ 2.3 units and SF-36 responders ≥ 4 units vs. baseline.


Eighty-five patients (78 chronic, 7 episodic) remained implanted and were evaluated for effectiveness at 12 months. In total, 68% of all patients were responders, 55% of chronic patients were frequency responders and 32% of all patients were acute responders. 67% of patients using acute treatments were able to reduce the use of these by 52% and 74% of chronic patients were able to stop, reduce or remain off all preventive medications. 59% of all patients were HIT-6 responders, 67% were SF-36 responders.


This open-label registry corroborates that SPG stimulation is an effective therapy for CH patients providing therapeutic benefits and improvements in use of medication as well as headache impact and quality of life.


Cluster headache; Long term effectiveness; Neuromodulation; Neurostimulation; Sphenopalatine ganglion
Lancet Neurol. 2018 Jan;17(1):75-83. doi: 10.1016/S1474-4422(17)30405-2. Epub 2017 Nov 23.

Diagnosis, pathophysiology, and management of cluster headache.


Cluster headache is atrigeminal autonomic cephalalgia characterised by extremely painful, strictly unilateral, short-lasting headache attacks accompanied by ipsilateral autonomic symptoms or the sense of restlessness and agitation, or both. The severity of the disorder has major effects on the patient’s quality of life and, in some cases, might lead to suicidal ideation. Cluster headache is now thought to involve a synchronised abnormal activity in the hypothalamus, the trigeminovascular system, and the autonomic nervous system. The hypothalamus appears to play a fundamental role in the generation of a permissive state that allows the initiation of an episode, whereas the attacks are likely to require the involvement of the peripheral nervous system. Triptans are the most effective drugs to treat an acute cluster headache attack. Monoclonal antibodies against calcitonin gene-related peptide, a crucial neurotransmitter of the trigeminal system, are under investigation for the preventive treatment of cluster headache. These studies will increase our understanding of the disorder and perhaps reveal other therapeutic targets.
[Indexed for MEDLINE]
Cranio. 1998 Jul;16(3):185-93.

Health care utilization by patients with temporomandibular joint disorders.


The claims data base of a large New England managed care organization was used to compare the health care utilization patterns of patients with TMJ disorders to non-TMJ subjects. Inpatient, outpatient and psychiatric claims data were examined over a wide range of diagnostic categories. Age and sex adjusted results showed that, overall, patients with TMJ disorders were greater utilizers of health care services and had higher associated costs than non-TMJ subjects. For some of the major diagnostic categories, such as nervous, respiratory, circulatory, and digestive, the inpatient and outpatient claims differences in utilization and costs were as large as 3 to 1. For only one diagnostic category, pregnancy and childbirth, were utilization and costs greater for non-TMJ subjects than TMJ patients. The psychiatric claims for TMJ patients exhibited differences that were at least twice as large as those for the non-TMJ subjects.
[Indexed for MEDLINE]

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posted by Dr Shapira at 3:43 PM

Friday, November 24, 2017

Patient describes treatment of her severe TMJ issues. She travels to Chicago for treatment.

Jen describes her treatment for chronic pain.


Ears ringing, Jaw Cracking, Jaw Pain, Myofascial Pain in head neck and ears, balance problems, tingling in my hands and feet,
I saw several dentists and was searching everywhere for an answer, I found Dr Shapira and e-mailed some of his former patients.
I have had oral appliance 2-2 1/2 months and it has made a huge diffence. I don't even think about my jaw anymore.
Prior to appliance it was even hard to eat.

With the appliance my balance is getting better.

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posted by Dr Shapira at 3:34 PM

The Sphenopalatine Ganglion (SPG) aka the Pterygopalatine Ganglion and it’s role in Pain Syndromes

This paper was originally published on the website:  www.SphenopalatineGanglionBlocks.com

There are also over 100 patient testimonial videos on SPG Blocks, Neuromuscular Dentry and Dental Sleep Medicine at:   https://www.youtube.com/channel/UCk9Bfz6pklC7_UluWFHzLrg/videos

The Sphenopalatine Ganglion (SPG) aka the Pterygopalatine Ganglion and it’s role in Pain Syndromes

I am going to go thru this excellent review paper and add my personal opinions based on almost 40 years of helping patients with chronic pain.  MY COMMENTS WILL BE IN ALL CAPITAL LETTERS:    THE ORIGINAL ARTICLE IS AVAILABLE ONLINE.
The Pterygopalatine Ganglion and its Role in Various Pain Syndromes: From Anatomy to Clinical Practice.
Maria Piagkou, MD, MSc, PhD*; Theano Demesticha, MD, PhD†
; Theodore Troupis, MD, PhD*; Konstantinos Vlasis, MD, PhD*; Panayiotis Skandalakis,
MD, PhD*; Aggeliki Makri, MD*; Antonios Mazarakis, MD, PhD*; Dimitrios
Lappas, MD, PhD*; Giannoulis Piagkos, MD*; Elizabeth O Johnson, MD, PhD*
*Department of Anatomy, Medical School, University of Athens, Athens; †
Department of
Anesthesiology, Metropolitan Hospital, P. Faliro, Greece
Abstract: The postsynaptic fibers of the pterygopalatine or sphenopalatine ganglion (PPG or SPG) supply the lacrimal
The PPG (SPG) appears to play an important role in various pain syndromes including headaches, trigeminal
and sphenopalatine neuralgia, atypical facial pain, muscle pain, vasomotor rhinitis, eye disorders, and herpes
Clinical trials have shown that these pain disorders can be managed effectively with sphenopalatine
ganglion blockade (SPGB). In addition, regional anesthesia of the distribution area of the SPG sensory fibers for nasal
and dental surgery can be provided by SPGB via a transnasal, transoral, or lateral infratemporal approach.  IF INJECTIONS  TO THE SPG ARE TO BE DONE THE SUPRAZYGOMATIC APPROACH TO THE INFRATEMPORAL FOASSA IS MOST EFFICATIOUS.
To arouse the interest of the modern-day clinicians in the use of the
SPGB (SPHENOPALATINE GANGLION BLOCK)  the advantages, disadvantages, and modifications of
the available methods for blockade are discussed.
Broad morphological and functional knowledge of the head anatomy is essential for neurology, neurosurgery,
and maxillofacial surgery practice. Nevertheless, there are areas and structures that still have not been
described or depicted sufficiently, owing to their small volume and complicated access. The pterygopalatine
ganglion (PPG), also known as sphenopalatine ganglion (SPG), Meckel’s or sphenomaxillary ganglion, OR THE NASAL GANGLION, OR SLUDER’S GANGLION is
located in the cranial section of the autonomic nervous System and bears unique characteristics favorable for
the treatment of many painful syndromes involving the face and head.1  THE GANGLIA IS LOCATED IN THE PTERYGOPALATINE FOSSA ON THE MAXILLARY DIVISION (V2) OF THE TRIGEMINAL NERVE.
SPG is located near important neuroanatomic structures for pain perception. Its proximity to multiple sensory facial and trigeminal branches.  THE SPG GANGLIA IS THE LARGEST PARASYMPATHETIC GANGLIA OF THE HEAD AND IT ALSO HAS SYMPATHETIC FIBERS RUNNING THRU IT.
Pain Practice 2011 World Institute of Pain, Pain Practice, Volume 12, Issue 5, 2012 399–41
PAI PRACTICE  suggests that SPG may be involved in persistent idiopathic facial pain (PIFP)2 and unilateral headaches.3 A
few motor nerves accompany the SPG sensory trunks.  THE AUTONOMIC NERVES RUN ALONG TRIGEMINAL NERVES.
An irritation of the SPG motor root may produce face and neck neuralgias by its connection
with the facial nerve (FN) , V7) lesser occipital and cutaneous cervical nervesN AND account for disturbances in the eye and mandible
region by its connections with the ciliary and otic ganglions and a variety of visceral symptoms by its connection with the vagus nerve.
EAR PAIN / OTALGIA THE AUTONOMIC NERVES  cause reflex otalgia by its connection with the
tympanic plexus.  THIS CONNECTION CAN ALSO CRERAT PAIN SYNDROMES EITHER PRODUCED BY SOUND OR NOISE OR WORSENED BY SOUND.  In addition, there may be motor phenomena of the soft palate related to the involvement of the motor
fibers to the levator palate and azygos uvulae muscles.  SPG has also been identified as the first relay station of
the autonomic fibers after emerging from the pons, suggesting that it may be used therapeutically in autonomic
imbalance situations.   SPG may play a critical role as a vasodilator to protect the brain against ischemia
The SPG as a major source for postganglionic parasympathetic fibers to the vascular beds of the cerebral hemispheres
is involved in tone regulation of the cerebral vessels.5 SPG’s communication with the superior cervical ganglion (SCG) (through the internal carotid
plexus) and the intracranial portion of the internal carotidartery (through its fibers from SPG) is related to edema, pain, dilatation, and low-grade encephalitis.6,7
SPG’s superficial location in the pharynx may explain
its sensitivity to odors, chemicals, and air particles.  SPG’s connection to the vagus nerve and the innervation
of the saliva producing glands predicts many of the digestive symptoms observed in dysfunctional
has highlighted the important role of the SPG in cerebrovascular autonomic physiology, in pathophysiology of cluster and migraine headaches, and in conditions
of stroke and cerebral vasospasm.9  IT SHOULD BE NO SURPRISE
The SPG, as THE LARGEST parasympathetic ganglion OF THE HEAD  is a nervous
mass of nervous tissues found in the course of the greater petrosal nerve (GPN) located deeply in the
pterygopalatine fossa (PPF). It is a small triangular or heart-shaped structure located close to the sphenopalatine
foramen (SPF) posterior to the middle turbinate and maxillary sinus, anterior to the medial plate of the
pterygoid process, and inferior to the sphenoid sinus and maxillary nerve (MN). IT IS ATTACHED TO THE MAXILLARY BRANCH OF THE TRIGEMINAL NERVE.  THE RECESS IS CALLED THE PTERYGOPALATINE FOSSA.
The SPG is morphologically configured in the last trimester of fetal life, and
during this period, its structure is established to ensure the nervous signal transmission.10 The SPG, a complex
neural center with multiple connections to trigeminal, facial, and sympathetic systems, consists of somatosensory, THE SOMATOSENSORY FIBERS ARE TRIGEMINAL AND MANY ARE PROPRIOCEPTIVE PASSING ON TH MESENCEPHALIC NUCLEUS, sympathetic (FROM SUPERIOR CERVICAL GANGLIA) , and parasympathetic fibers (FROM SPG NERVE CELLS) and receives a sensory, motor, and sympathetic root. The SPG sensory root is derived from two pterygopalatine branches of the MN; their fibers pass directly into the palatine nerves, and a few enter the SPG constituting its sensory root. The sensory distribution to the nose, throat, and sinuses gives characteristic indications in these regions.11 The SPG motor root probably derived from the nervus intermedius (glossopalatinus or nerve of Wrisberg) through the greater superficial petrosal nerve (GSPN) and may consist of sympathetic efferent (preganglionic) fibers from the medulla. SPG motor fibers form synapses with neurons whose postganglionic axons are distributed with the deep branches of the trigeminal nerve (TN) to the mucous membrane of
the nose, soft palate, tonsils, uvula, roof of the mouth,
upper lip, and gums and to the upper part of the pharynx.12
The SPG autonomic innervation is more complex.
The SPG sympathetic root is derived from the
internal carotid plexus through the deep petrosal nerve
(DPN). The GSPN and the DPN join to form the nerve
of the pterygoid canal (vidian nerve) before entering
the SPG. The SPG parasympathetic root has its preganglionic
origin in the superior salivary nucleus. The preganglionic
fibers pass through nervus intermedius, FN,
geniculate ganglion, and greater petrosal nerve reaching
the ganglion via nerve of pterygoid canal. The
GSPN carries taste along with the presynaptic parasympathetic
fibers. The taste fibers pass through the
SPG to the soft palate, while the parasympathetic
fibers synapse in the SPG and postsynaptic fibers supply
the lacrimal gland, mucosa of the palate, nasopharynx,
and nasal cavity.13
The DPN, a branch of the internal carotid plexus
(the continuation of the cervical sympathetic trunk in
the cranium), carries postganglionic sympathetic fibers
from the SCG. The postganglionic sympathetic nerve
fibers pass through the SPG without synapsing and join
branches of the MN, which distributes to the nasal
cavity, palate, and upper pharynx. The GSPN and
DPN (join at the foramen lacerum to form the vidian
nerve) pass forward, through the pterygoid canal, with
the corresponding artery, and joined by a small
ascending sphenoidal branch from the otic ganglion.
Finally, vidian nerve enters the PPF and joins the posterior
angle of the SPG14 (Figure 1).
The nerves of the SPG are predominantly composed of
MN sensory fibers. Several delicate orbital branches of
the pterygopalatine nerves enter the orbit via the inferior
orbital fissure to supply the orbital periosteum and
muscle, and the mucous membrane of the posterior ethmoid
and sphenoid sinuses. The three palatine nerves,
the one greater (anterior palatine nerve) (GPN) and two
lesser (middle and posterior) palatine nerves (LPN), exit
the SPG inferior surface to descend behind the perpendicular
plate of the palatine bone. The anterior or GPN
descends through the pterygopalatine canal (PPC)
accompanied by the descending palatine artery. Emerging
onto the oral palatal surface at the greater palatine
foramen (GPF), it passes anteriorly, medial to the alveolar
bone process giving branches to mucosa and glands
of the hard palate, as far as the incisor teeth. The GPN
communicates in the incisive canal region with a branch
of the nasopalatine nerve. Posterior inferior lateral
nasal branches of the GPN leave the nerve in the PPC
and enter the nasal cavity to supply the middle and inferior
meatuses and the inferior concha. Several posterior
superior lateral nasal branches of the PPG pass through
the SPF into the posterior part of the nasal cavity and
distribute to the superior and middle nasal conchae, the
posterior ethmoidal air cells, and the posterior part of
the septum. The middle and posterior or LPN penetrate
the hard palate via the lesser palatine foramina (LPF) to
supply the soft palate, uvula, and tonsils. In addition,
taste receptors of the palate are innervated by special
visceral afferent fibers of the FN that are carried by the
GPN and LPN, back through the PPG and the greater
petrosal nerve to the geniculate ganglion. The nasopalatine
nerve (the larger of the posterior nasal branches)
passes across the roof of the nasal cavity to the septum
and runs inferiorly and anteriorly on the inclined edge
of the vomer, supplying the septum. At the incisive
canal, the two nasopalatine nerves descend to the palate,
communicate with the terminals of the anterior palatine
nerves, and consequently participate in the
innervation of the upper central incisors. Finally, the
pharyngeal nerve leaves the SPG posterior part and
enters the pharynx via the palatovaginal canal with a
pharyngeal branch of the maxillary artery (MA) to
reach the sphenoid sinus and nasopharynx behind the
auditory tube15(Figure 2).
Sphenopalatine ganglion blockade has been achieved
with a variety of methods, for various pain disorders,
when more conservative treatments have failed. In
1908, Sluder proposed that a high-grade inflammatory
reaction in the posterior ethmoid and sphenoid sinuses
may be involved in certain cases of unilateral facial pain
associated with lacrimation, rhinorrhea, and mucosal
congestion. These symptoms are associated with the
extension of inflammation or the transmission of toxins
into the SPG.16 Sluder reported that patients who had
refused surgery for an active ethmo-sphenoid inflammation
later developed sphenopalatine ganglion neuralgia
(SPGN). He also claimed success in relieving the symptoms
of facial neuralgia, asthma,17 earache,18 and
lower-half headache19 using ablation. Ruskin described
Figure 1. Parasympathetic preganglionic axons derived from
the facial nerve leave the main trunk of the nerve and course as
the greater superficial petrosal nerve. Sympathetic postganglionic
axons derived from cell bodies in the superior cervical ganglion
(SCG) course on the ICA surface and enter the skull with
the artery at the carotid canal. The sympathetic axons course
through the adjacent sphenopalatine ganglion (SPG) without
synapsing and are distributed with the nerve and arterial
branches emanating from it, to the nasal and pharyngeal
mucosa. The parasympathetic fibers entering the SPG synapse
there and distribute to glands in the same mucous membranes.
Some of the postganglionic axons pass to the lacrimal gland by
way of first the maxillary nerve, then 1 of its branches, the
zygomatic nerve, and finally by way of 1 of the branches of the
ophthalmic division of the trigeminal nerve, the lacrimal nerve.
Sources: Adapted from Basic Human Anatomy – O Rahilly, Muller,
Carpenter and Swenson (on line darmouth.edu).
PPG and its Role in Pain Syndromes • 401
the technique with cocaine for the treatment of chronic
muscle spasm,20 arthritis,21 and polyarthritis,22 and
Ruskin A.P. used pentocaine for a variety of other conditions.23
Barre24 described a SPGB method using a
dropper to instill local anesthetic into the nose, but
much of the anesthetic was absorbed throughout the
nasopharynx without reaching the SPG. Hardebo and
Elner25 reported that SPGB can be used as an abortive
historically employed for various pain syndromes,
many of these reports are anecdotal and remain controversial.6,26–28
Diagnostic and therapeutic head and neck blocks can
also assist with the diagnosis and management of
many chronic pain conditions (pain of musculoskeletal,
vascular, and neurogenic origin).29 Currently
accepted indications for the SPGB include: SPG and
trigeminal neuralgia (TGN), PIFP (previously referred
to as atypical facial pain), acute migraine, acute and
chronic CH, herpes zoster involving the ophthalmic
nerve, and a variety of other facial neuralgias12,29–31
Sphenopalatine ganglion neuralgia or Sluder’s neuralgia
(SPGN) is a type of facial neuralgia, defined as a
symptom complex consisting of neuralgic, motor, sensory,
and gustatory manifestations.32 SPGN could be a
trigeminal autonomic cephalalgia (TAC), described as
unilateral facial pain in the orbital region that sometimes
spreads retro-orbitally toward the zygoma and
extends posteriorly to the mastoid and occiput.33
SPGN refers to intermittent episodes of vasomotor
hyperactivity causing conjunctival injection, lacrimation,
serous nasal discharge and unilateral nasal mucosal
inflammation, and sensory disturbances of the
palate and oropharynx with distorted gustatory sensations.
Occasionally, SPGN is a bilateral constant pain
with exacerbations or a pain that stopped and reappeared
cyclically or with stabbing sharpness. The pain
is typically associated with anesthesia of soft palate,
pharynx, tonsils and nose, and hyperesthesia along the
distribution of the TN. The parasympathetic signs are
ipsilateral lacrimation, conjunctival injections, nasal
obstruction, rhinorrhea, serious nasal discharge, or
mucosal congestion34,35 (Table 1).
Trigeminal neuralgia, also called ‘‘tic douloureux,’’
is a peculiarly painful paroxysmic disorder that undergoes
spontaneous remissions and recurrences. The
pain, subserved by large fibers, can be triggered from
outside the trigeminal territory and by other factors
than mechanical stimuli. There are strong autonomic
influences of the pain, and there is a cutaneous vasoconstriction
in the trigeminal territory in which it
Figure 2. The sphenopalatine ganglion and its connections—communications
of the PPF. SPF, sphenopalatine foramen;
FR, foramen rotundum; PhC, pharyngeal canal; PtC,
pterygoid canal; PPF, pterygopalatine fossa.
Source: Adapted from Google pictures database (95 1252 pair.-
Table 1. Sphenopalatine ganglion blockade (SPGB) in the Treatment of Sluder’s Neuralgia
Authors Patients Technique Efficacy
Salar et al.35 7 Percutaneous radiofrequency thermocoagulation
1/10 needed repeat lesioning
2/10 needed additional RFTC
Pollock and
1 Stereotactic radiosurgery targeted at the
SPG—repeated radiosurgery 17 months later for
partial pain recurrence
2 years pain-free (without nasal discharge or
eye irritation)
Puig and Driscoll37 8 13 occasions of SPG (88% phenol) intranasal 90% decrease in head and face pain (for an
average of 9.5 months). The recurrent pain
was less severe, less frequent and of shorter
et al.38
3 4% xylocaine intranasally and intranasal
Total relief of pain
Karas et al.33 1 SPG gamma knife radiosurgical ablation Total relief of pain
occurs.39 TGN manifests as severe disabling facial pain
unilaterally either episodic or chronic and is most common
in older people than 50 years of age and in
women.40,41 Pain paroxysms can be precipitated by
nonpainful stimuli (touch, movement, wind exposure,
chewing, brushing teeth, shaving, and swallowing) in 1
or more branches of the 5th cranial nerve.13,41 The
pain is of much shorter duration than that of CH, but
sometimes, it can be associated with CH giving rise to
a ‘‘cluster tic.’’ Atypical TGN encompasses various
facial pain syndromes including those arising from
dental or otorhinolaryngological disorders. Paroxysmal
hemicrania (PH) belongs to TACs with severe strictly
unilateral pain attacks localized to orbital, supraorbital,
and/or temporal sites accompanied by 1 or more
ipsilateral autonomic features.40,42 SPGB could be considered
a reasonable alternative in drug-resistant PH
cases where indomethacin is contraindicated. Several
treatment options are available (Table 2).
Cluster headache (CH) is relatively uncommon and
the most painful form of recurring primary neurovascular
headache. CH has been described with a variety
of names, including histamine cephalgia (Horton headache)
and paroxysmal nocturnal cephalgia.49 CH is a
severe, strictly unilateral head pain (ocular, frontal,
and temporal) in the territory of the TN distribution,
associated with autonomic manifestations homolateral
to the pain and usually follows circadian and circannual
patterns. The autonomic manifestations seem to be
both parasympathetic (lacrimation and rhinorrhea)
and sympathetic (ptosis and miosis). The periodicity of
the attacks and seasonal recurrence of the cluster periods
suggest the involvement of a biologic clock within
hypothalamus.50 CH is characterized by a constant
unilateral orbital location and tends to recur nightly at
the same time and last for 6 to 12 weeks, followed by
complete freedom from headache for months or even
years. The associated autonomic phenomena of a
blocked nostril, rhinorrhea, injected conjunctivae, lacrimation,
ptosis, miosis, and flushing of the cheek are
frequently present. This headache typically responds at
least initially to medication. The pathophysiology of
CH involves the activation of parasympathetic nerve
structures located within the SPG, which explains
many of the associated symptoms (conjunctival injection,
lacrimation, nasal congestion, rhinorrhea, forehead
and facial sweating, miosis, ptosis, or eyelid
edema).51 The prominent cranial autonomic symptoms
may be due to central disinhibition of the trigeminovascular
autonomic reflex by the hypothalamus,
possibly through direct hypothalamic-trigeminal
connections.42 Communication between the SPG and
the V2 TN has also been described as a mechanism
responsible for CH.52
The International Headache Society (HIS) divided
CH into groups according to they include: CH periodicity
undetermined; episodic; and chronic CH (unremitting
from onset or evolved from episodic)
(Headache Classification Subcommittee).53About 90%
of people with CH have the episodic form, but 10%
have chronic CH (the attacks occur for more than 1
year without remission or with remissions lasting
< 1 month).42 Attacks occur in CH which follows a chronobiological pattern that appears to coincide with the seasonal change in the length of day. During a cluster period, headaches occur 2 to 3 times daily for Table 2. Sphenopalatine ganglion blockade (SPGB) in the Treatment of Trigeminal Neuralgia Authors Patients Technique Efficacy Manahan et al.43 1 10 treatments (bupivacaine 0.5%) Pain-free for 30 months Spacek et al.44 39 17 patients (carbamazepine and apuncture therapy) (group A) 11 patients (carbamazepine local ganglionic opiod analgesia (GLOA) and apuncture therapy (group B) 11 patients carbamazepine and GLOA without apuncture (group C) GLOA was carried out with 0.045 mg buprenorphine at the superior cervical ganglion or at the SPG 8 patients of group A, 5 of group B, and 2 of group C remained pain-free Most patients with no improvement were from group C Saberski et al.45 1 11 times repeated therapy (transnasal approach) Bradycardia was resolved with successful alleviation of pain Gre´goire et al.46 1 3 separate CT-guided injections Pain-free Kanai et al.47 25 2 sprays (0.2 mL) of either lidocaine 8% or saline placebo in the affected nostril using a metered-dose spray. Intranasal lidocaine 8% spray decreased symptoms. Pain was described as moderate or better by 23 patients of the lidocaine spray and 1 of the placebo group. Zarembinski and Graff-Radford48 26 SPGB fluoroscopically on 12 patients that responded to stellate ganglion blocks and 14 additional patients 20 of 26 patients responding to SPGB (76.9%) PPG and its Role in Pain Syndromes • 403 45 minutes to 1 hour. The SPG seems to play a very important role in pathology. It is hypothesized that SPGB relieves headaches because it breaks the vicious autonomic cycle of pain within the facial and cranial area54,55 (Table 3). Migraine headache is an intensely unilateral, periorbital severe pain. The perception of migraine headache is formed when nociceptive signals originating in the meninges are conveyed to the somatosensory cortex through the trigeminal ganglion, medullary dorsal horn, and thalamus. Different migraine triggers activate a wide variety of brain areas that impinge on parasympathetic neurons innervating the meninges. Migraine triggers either activate or originate in a number of brain areas whose projections converge on the superior salivatory nucleus. The superior salivatory nucleus, in turn, activates postganglionic parasympathetic neurons in the SPG, resulting in vasodilation and local release of inflammatory molecules that activate meningeal nociceptors. Typically, migraine headache is a unilateral pain beginning most commonly in frontotemporal area that may involve whole hemicranium, alternating sides between or during an attack. It is associated with depression, stress, hunger, fatigue, sleepiness, anorexia, nausea, vomiting, photophobia, and phonophobia. Redness and swelling of the mucous membrane of the nose and conjunctival injection may also occur with migraine70,71 (Table 3). In recent years, SPG neurolysis after successful blockade has been utilized in such cases with varying success.34,51,57,58,72 SPG neurolysis is indicated for PIFP,2 previously known as atypical facial pain. PIFP is defined as a constant, deep, and pulling or crushing pain in the head or face, present all or most of the day, which may become more intense during exercise. Pain is most often localized to the maxilla and may extend to the region of the eyes, nose, cheek, and temple.73 Patients who have PIFP syndromes (after trauma, surgery, or on an idiopathic basis) are more difficult to treat than those with typical TGN.58 The pathophysiologic mechanism remains unknown, and the cause is likely to be multifactorial.57 Remick et al.74 reported a 68% incidence of psychiatric disorders in patients with PIFP, but PIFP cannot be related to a psychiatric disorder. If symptoms make it impossible to determine the pain origin or if they do not guide the clinicians toward any other facial pain syndrome, then the diagnosis is a PIFP.75 PIFP may have a sympathetic component, which makes neurolysis of the SPG ideal as the postganglionic sympathetic nerves pass through the ganglion. Pulsed radiofrequency (PRF) treatment of the SPG can be considered with a maximal temperature of 42C for 1 or for more times during a period of 120 seconds.2 Head, Neck, Shoulders Pain, and Complex Regional Pain Syndromes6 Because the C2, C3, and C4 cervical roots are connected to the SCG and through the DPN to the SPG, the SPGB is able to relieve pain not only from the head, face, neck, and upper back but also diminishes the symptoms from the head and face, which are attributed to the upper cervical spine. The first successful SPGB for myofascial pain originating in the trapezius and sternocleidomastoid muscles was reported by Ruskin.76 Since then, other authors have asserted potential applicability for SPGB in the treatment of myofascial pain and fibromyalgia77,78 while others question the therapeutic applicability of SPGB for myofascial pain (Table 4). Head and Neck Advanced Malignancies Pain resulting from head and neck cancer can be severe and difficult to manage. In certain patients, SPGB can be effectively self-administered at home to manage chronic pain.81 Prasanna and Murthy82 have been used SPGB as an adjunct therapy for immediate relief from pain in the ear arising from the floor of the mouth and extensive tongue lesions because of malignancy (Table 5). Recently, SPGB has been applied for the treatment of musculoskeletal pain, especially that of the neck and back.28,31Although various studies with SPGB for management of low back pain have used cocaine,21 pentocaine,27 and 4% topical xylocaine28 with some success, these conditions are not yet considered among the primary indications. TECHNIQUES FOR SPHENOPALATINE GANGLION BLOCKADE (SPGB) The techniques for SPGB range from superficial to highly invasive. The drugs frequently used are local anesthetics (4% cocaine, 2% to 4% lidocaine, or 0.5% bupivacaine), depot steroids, or 6% phenol. To prolong the SPGB, radiofrequency thermocoagulation (RFT) can be employed. PRF has gained interest as a method. Because it is delivered in pulses, followed by a silent period, allows adequate time for dissipation of heat and energy, resulting in less damage to surround- 404 • PIAGKOU ET AL. Table 3. Sphenopalatine ganglion blockade (SPGB) in the Treatment of Cluster Headache (CH) and Facial Pain Authors Patients Syndrome Technique Efficacy Devoghel54 120 CH Alcohol infiltration Relief of pain > 85%
Onofrio and
26 Chronic CH Posterior fossa trigeminal
rhizotomy or percutaneous
radiofrequency trigeminal
ganglion rhizolysis
54% excellent relief of pain, 15% fair
to good relief of pain, 31% poor relief
Cepero et al.57 12 Facial pain SPG neurectomy High incidence of pain recurrence
Stechison and
4 Post-traumatic PIFP Transfacial transpterygomaxillary
access to foramen rotundum,
SPG, and maxillary nerve
3 patients (complete pain relief)
1 patient free of pain for 12 months
1 patient free of pain for 5 months
Taha and
7 Chronic CH Percutaneous stereotactic
radiofrequency rhizotomy
Long pain relief
Sanders and
66 Episodic CH (56 patients)
Chronic CH (10 patients)
Radiofrequency lesioning in the
SPG (infrazygomatic approach)
Complete relief of pain in 34 patients
of ECH (60.7%) and in 3 patients of
CCH (30%) and no relief in 8 patients of
ECH (14.3%) and in 4 of CCH (40%)
Maizels4 1 Recurrent headache
(migraine with aura)
Intranasal lidocaine 4% during
the aura phase
The headache following the aura was
prevented and remained successful on
all but 2 occasions over 1.5 years
Costa et al.60 15 Episodic CH (6 patients)
Chronic CH (9 patients)
10% solution of cocaine
hydrochloride or 10% lidocaine or
saline under anteriorrhinoscopy
All patients responded promptly to both
anesthetic agents, with complete
cessation of induced pain. In the case
of saline application, pain severity
Krasuki et al.61 15 Severe headache
head trauma (7 patients)
dental work (2 patients)
herpes zoster (2 patients)
fibromyalgia (1 patient)
pharyngitis (1 patient)
migraine (1 patient)
unkown reason (1 patient)
SPGB with sterile cotton sticks,
soaked in 4% lidocaine, inserted
through the patient’s nose to the
back of nasopharynx for 10
minutes, daily for a week
In 12 of 15 patients, the pain was
Yarnitsky et al.62 Migraine SPGB by applying lidocaine
Mean pain score was 7.5 of 10 during
untreated migraine and 3.5 of 10 after
the SPGB. Cutaneous allodynia
remained despite the pain relief
Shah and
1 Post-traumatic headache SPG pulsed-mode radiofrequency
Pain relief more than 17 months
Bayer et al.64 46 Chronic face and head pain
(various aetiologies)
SPG pulsed-mode radiofrequency
lesioning (procedure was repeated
in 20% of the patients)
65% mild-to-moderate pain relief 14% no
pain relief and 21% complete pain relief
De Salles
et al.65
5 Classic unilateral CH
(1 patient)
neuropathic pain
(2 patients)
bilateral migrainous
neuralgia (1 patient)
bilateral PIFP (1 patient)
Radiosurgery of the SPG with a
single maximal dose of 90 Gy with
a 5- or 7.5 mm circular collimator
Only the patient with CH experienced
lasting pain relief
Felisati et al.66 21 Chronic drug-resistant CH Endoscopic SPG via the lateral
nasal wall
Treatment was inapplicable a cause
nasal stenosis (1 patient)
complete disappearance of the attacks
(8 patients) a partial benefit (3 patients)
no response (9 patients)
Yang and
1 Chronic, left-sided CH Topical anesthesia to the nasal
mucosa, followed by a needle
insertion guided by its tailored
plastic cover-sheath for injecting
blocking agents
Pain-free for 1 week, 60% pain reduction
with less frequent episodes and easily
controlled with abortive medicine for
3 weeks
Tepper et al.68 11 Intractable migraine SPGB using the infrazygomatic
transcoronoid approach under
fluoroscopy guidance
2 patients—pain-free
3 patients—pain reduction
5 patients—no response
1 patient—was not stimulated
et al.69
15 Chronic CH SPGB via infrazygomatic approach
under fluoroscopic guidance
3 patients—no response
7 patients—pain reduction
3 patients—pain-free
2 patients—complete relief of pain
PPG and its Role in Pain Syndromes • 405
ing structures.88,89 More recently, electromagnetic
field-pulsed radiofrequency lesioning (EMF) has been
used. The current hypothesis on the mechanism of
EMF action is that the nerve membrane has a capacitor
function and EMF creates a high electric field,
which punches holes in the capacitor, thus blocking
transmission of stimuli through A-delta and C-fibers.90
The Intranasal Approach
The intranasal application of topical anesthetic is the
simplest and most tolerable technique. Cocaine or lidocaine
is placed on the nasopharyngeal mucosa posterior
to the middle turbinate, using a cotton-tipped
applicator. The zygomatic arch is taken as a reference,
because it is parallel to middle turbinate. However, the
topical anesthetic diffusion to the SPG is unpredictable,
and the SPGB is not durable.67 Nose abnormalities
can make this route difficult, uncertain, and
sometimes dangerous.11 Several modifications of the
traditional intranasal technique have been described.
Mingi91 modified the technique by using an intratracheal
cannula, instead of a cotton applicator, for better
patient tolerance. Varghese et al.92 combined both the
Table 4. Sphenopalatine ganglion blockade (SPGB) in the Treatment of Myofascial Pain (Fibromyalgia and Pain from
the Area of Head, Neck, and Shoulders)
Authors Patients Technique Efficacy
Scudds et al.79 61 Insertion of 2 soaking pledgets (lidocaine 4%
or sterile water) under direct vision,
6 times over a 3-week period
21 patients (35%) decrease in pain (> 30% of their
baseline value). Of these 21, 10 had received lid
and 11 placebo 4% lid is no better than
placebo in the treatment of chronic muscle pain
Ferrante et al.6 23 4% lidocaine, then TPI with 1% lidocaine, and
finally SPGB with saline placebo
or SPGB with saline placebo, then TPI with 1%
lidocaine, and finally SPGB with 4% lidocaine
SPGB with 4% lidocaine is no more efficacious
than placebo and less efficacious than administration
of standard trigger point injections (TPI)
Quevedo et al.80 2 One culturette swab dipped in 4% tetracaine,
in each nare, is advanced gently under the
inferior turbinate until it reaches the area of
the branch of the SPG. After 10 to
15 minutes, the culturettes are removed
Both patients experienced a 50% reduction in pain
Table 5. Sphenopalatine ganglion blockade (SPGB) in the Treatment of Other Pain Syndromes
Authors Patients Syndrome Technique Efficacy
Slade et al.83 13 Tear secretion Topical anesthesia (proparacaine 0.5%,
followed by lidocaine 2%)
Tear secretion was reduced substantially or
stopped completely after SPGB
et al.84
17 Nicotine addiction Intranasal application of bupivacaine,
cocaine, or saline
Significantly fewer symptoms of physical
discomfort in the anesthetic treatment
Prasanna and
30 Chronic vasomotor
Bilateral SPGB 29 patients—no recurrence of symptoms
(follow-up 12 to 20 months)
1 patient—symptom-free (for 8 months)
Robiony et al.85 12 Skeletal transverse
discrepancy of the
Transcutaneous truncal anesthesia of
the maxillary nerve in association with
transmucosal anesthesia of the SPG
(lidocaine-prilocaine cream)
The maxillary anesthesia facilitated the
operations and reduced the amount of
postoperative pain
Hilinsky et al.86 1 Post-traumatic
fluid rhinorrhea
Restore the normal autonomic
homeostasis in the nasal cavity either
with topical medicines or with surgical
procedures aimed at disruption of
parasympathetic preganglionic fibers
proximal to or at the SPG
Varghese et al.87 22 Head & neck
cancer pain
Nasal endoscopically guided neurolytic
SPGB with 6% phenol
17 patients had good immediate relief,
1 patient had partial relief, and 4 patients
reported inadequate relief
Prasanna5 1 Hyperhydrosis 2 SPGB at weekly intervals 50% reduction in the sweating with the
first block, and 90% improvement with
the second block. In a follow-up of
12 months, there was no recurrence.
Windsor and
1 Eye pain due to
herpes keratitis
The patient experienced a month of relief
before the pain returned
principles of external approach for neurolytic and surface
SPGB for pain owing to advanced head and neck
cancer. Windsor and Jahnke30 attempted to control
the medication amount reaching the posterior nasopharynx
as well as provide better needle guidance.67
The increased danger to the nasal mucosa during needle
insertion led to the development of the transnasal
endoscopic technique, where the needle is inserted
under direct vision, using rigid sinuscope. Recently, Felisati
et al.66 described an endoscopic SPGB technique
that approaches the PPF via the lateral nasal wall.
Overall, intranasal topical application is not invasive
and should be attempted before submitting patients to
more invasive surgical approaches. Once a patient
experiences good pain relief, repeat blocks are performed
before finally deciding on SPG radiofrequency
lesioning (RF). A RTFC or EMF procedure can be performed
for prolonged analgesia. The use of phenol for
neurolysis via this approach is not recommended
because of the possibility of inadvertent spread of the
phenol into surrounding tissues.13
The Transoral Approach (Greater Palatine Foramen
Injection through the pterygomaxillary fissure has
been commonly used by dentists for tooth extractions
and routine periapical surgery in the anterior maxillary
region. The intraoral route is the most direct, dif-
ficult, uncertain, and occasionally impossible to reach
the SPG11 and exhibits the greatest complications. Via
this approach, a curved dental needle passes through
the GPF at the posterior portion of the hard palate
just medial to the gum line opposite the third molar
tooth to reach the superior aspect of the PPF67 where
the main trunk of the maxillary division of the TN
lays.93 Paresthesia may be induced because the MN is
just cephalad to the SPG. The SPGB via this route is
extremely painful for the patient because the needle
passes through the canal that contains a nerve trunk,
artery, and vein and the anesthetic solution is deposited
into a space that has very little compliance.94
Because of the high vascularity of the region, an intraorbital
hematoma may result from injecting local anesthetic
in the terminal branches of the MA,77 which
follow the distribution of the terminal branches of the
MN. Infiltration of the PPF through the GPF approach
may result in infraorbital nerve injury and anesthesia
or injury of the orbital nerves.93 Another significant
disadvantage may be the difficulty in correctly identifying
the GPF, as the needle may not stop automatically
on the sphenoid bone and pass beyond the
sphenoid buttress to anesthetize other structures.67
Because the GPC and hard palate form an angle of
approximately 60,
95 it has been suggested to bend the
needle 45 to facilitate the passage of the needle
through the GPC and to prevent it from penetrating
too far into the PPF. There is no data on standard radiofrequency,
EMF lesioning, or phenol injection of
the SPG via this approach.90
The Infrazygomatic Arch (Lateral Infratemporal)
The infrazygomatic approach is necessary to perform
the majority of neurolysis techniques. The infrazygomatic
approach has been commonly performed blindly,
without C-arm fluoroscopic guidance, but it is highly
recommended using fluoroscopy. The approach is carried
out by using C-arm fluoroscopic guidance and a
direct lateral approach to place a cannula into the
superior portion of the PPF without requiring local
anesthetic to diffuse across mucous and bony membranes
and does not rely on secondary spread via the
nerves of the GPC.3,67
A transfacial transpterygomaxillary technique in the
region of foramen rotundum can be used to block the
MN and the SPG. For this, a spinal needle is inserted
at the intersection site of a vertical line extending
along the lateral orbital wall and a horizontal line tangential
to the lateral aspect of the inferior surface of
the zygomatic process of the maxilla. The procedure is
guided by CT scan to confirm the final needle position
or to guide fine adjustments in position. The used CT
scan helps avoid inadvertent passage of the needle
through the inferior orbital fissure into the intraorbital
contents or even the globe. This technique is indicated
for PIFP in the MN distribution. The advantage is that
allows the needle to be oriented more closely to the
axis of the foramen rotundum and the MN.58
The intimate relationship between the SPG and traversing
second-division trigeminal branches explains
the majority of potential complications following SPG
lesioning. SPGB is not a benign procedure, and infection
is possible if proper aseptic technique is not followed.
Nasal epistaxis can occur if the practitioner is
not careful when placing the cotton-tipped applicators
PPG and its Role in Pain Syndromes • 407
into the nasal passageway or if too much pressure is
applied from the needle to the lateral nasal wall.13
Epistaxis occurs more often during winter months,
when forced air heating may cause drying the nasal
mucosa. Complications associated with any invasive
craniocervical procedure, include hemorrhage, failure
to relieve pain, worsening of pain, nontarget nerve
injury, blindness, paralysis, stroke, seizures, and death,
although the risk of devastating complications in experienced
hands is remote.3 The use of chemical, surgical,
cryolysis, and thermocoagulation neurolysis
methods may not be the ideal strategy to treat noncancer
pain, because of the possibility of damaging vital
In contrast to the neurolytic procedures, pulsed radiofrequency
lesioning (PRF) provides long-term pain
relief without destroying neural tissue and has been
incorporated into existing percutaneous techniques for
craniofacial pain syndromes.96 In PRF, the impact of
electric field on the neuronal cells is well accepted; the
high-density electrical field generated around the RF
electrode tip is hypothesized to induce changes in the
nerve cells responsible for an altered pain signal transmission.
In PRF where the electrical current is delivered
in pulses, the heat generated is desipated during
the silent periods, suggesting that local heat induction
may not play a significant role. On the other hand,
PRF was found to induce a significant transient inhibition
of evoked excitatory transmission, and PRF activity
appears to be selective for small diameter (C and
Ad) axons that play a primary role in nociception.88
Radiofrequency lesioning (RF) of the SPG is performed
for 70 to 90 milliseconds at 67 to 80C. The mechanism
of action of RF has not been completely resolved.
There is some evidence that a heating effect induced by
the current may be involved, at least, in a part.97 However,
there is also growing evidence suggesting that the
high-density electrical field generated around the electrode
may alter neuronal activity and subsequently
alter pain transmission. PF can result in permanent or
more commonly temporary hypoesthesia, dysesthesia,
or differentiation pain in the palate, maxilla, or posterior
pharynx.98,99 Hematoma formation can occur after
injury of the MA large venous plexus, which lies
within the PPF following intravascular injection.100
(Figure 3). Cheek hematoma and infection are always
a possibility especially if the oral or nasal mucosa was
accidentally penetrated. Attention must be paid to the
total dose of local anesthetic used if toxic effects are to
be avoided.101
Complications associated with SPGB or neurolysis
include injury to the MN and MA, perforation of the
nasal wall and orbit, bradycardia, hemodynamic instability,
toxicity, nasal bleeding, facial hematoma and
numbness of the upper teeth, hard palate, or pharynx.
Intranasal sensory changes are rarely noticed. These
complications may be minimized if sharp needles are
replaced with curved-blunt needles and standard neurolysis
is replaced with pulsed radiofrequency lesioning.63
Recently, it has been noted in some patients,
reflex bradycardia (referred to as the ‘‘Konen reflex’’)
has been observed during radiofrequency treatment of
the SPG. In these cases, the lesioning was halted and
the bradycardia resolved.13,102
Sphenopalatine ganglion blockade has been performed
for the past 90 years. The role of the SPG in the pathogenesis
of pain still remains debatable. Although the
effectiveness and duration of SPGB can vary, usually
depending on the patient, SPGB can be rewarding,
safe, and lasting intervention in the treatment of a
wide range of environmental sensitivity disorders and
illnesses. A thorough understanding of the anatomy
allows clinicians to predict correct needle placement
and may reduce the incidence of complications. The
Gasserian ganglion
Figure 3. Anatomical lateral view of the pterygopalatine fossa
(PPF), which houses the maxillary artery (MA), the sphenopalatine
ganglion, and the MN. The (PPG) lies deeply in the fossa.
The sphenopalatine artery (SPA) is the end artery of the MA
located within the PPF and passes through the sphenopalatine
foramen on lateral nasal wall. Nasal bleeding from this artery is
potentially life threatening and may urgently require endonasal
endoscopic occlusion.100
Source: Adapted from Google Database (on line darmouth.edu).
search for the precise technique continues, and the currently
available evidence should be completed with
well-designed trials.
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