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Abstract
There is renewed interest in the central role of the sphenopalatine ganglion (SPG) in cerebrovascular autonomic physiology and the pathophysiology of different primary and secondary headache disorders. There are diverse neural structures (parasympathetic, sympathetic and trigeminal sensory) that convene into the SPG which is located within the pterygopalatine fossa (PPF). This makes the PPF an attractive target to neuromodulatory interventions of these different neural structures. Some experts advocate for the nasal application of local anesthetics as an effective route for SPG block with the belief that the local anesthetic can freely access the PPF. It is time to challenge this historical concept from the early 1900s. In this daring discourse, I will review anatomical studies, CT and MRI reports to debunk this old myth. Will provide anatomical evidence to explain that all these assumptions are untrue and the local anesthetic has to magically ‘travel’ a distance of 4–12 mm of adipose and connective tissue to reach the SPG in sufficient concentration and volume to effectively induce SPG blockade. Future research should focus on assessing a clinical biomarker to confirm SPG blockade. It could be regional cerebral blood flow or lacrimal gland secretion.
- anesthesia
- local
- autonomic nerve block
- pain management
- post-dural puncture headache
- education
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Introduction
The pterygoplatine fossa (PPF) is a natural crossroad situated between the maxillary, sphenoid and palatine bones. Located in the PPF is the sphenopalatine ganglion (SPG), which is the largest peripheral parasympathetic ganglion. The SPG is primarily a parasympathetic ganglion, however, it also transports sensory and sympathetic fibers which—in contrast to the parasympathetic fibers—pass through the ganglion without synapsing. This neural network makes the SPG an important target for modulation of these neural pathways in the management of primary headache disorders (migraines, cluster headaches, trigeminal autonomic cephalalgia) and secondary headache disorders (postdural puncture headache (PDPH) and post-traumatic headache, postherpetic trigeminal neuralgia).1 SPG stimulation can lead to increased regional cerebral blood flow and reverse cerebral vasospasm.2–4 Cerebral vasodilation occurs through the release of different neurotransmitters, mainly acetylcholine, vasoactive intestinal peptide and nitric oxide.5 6
Recently, there is a renewed interest in using SPG block, through the application of intranasal local anesthetic (LA), for the management of headaches in general and PDPH specifically,7 Advocates for this approach promote this practice as a simple and effective tool, however, current evidence is mixed and indecisive.
To consider intranasal LA application as SPG block is in fact groundless and unfounded, as simply we do not have a clinical biomarker to validate an effective SPG block.
One must accept too many assumptions to consider topical intranasal application as SPG block. First, assume that most of the nasally applied LA is not being swallowed. Second, the remaining few drops of LA can passively diffuse through the nasal mucosa and the sphenopalatine foramen (SPF), Third, the SPG lies directly under the nasal mucosa.
SPG neuroanatomy
The SPG is primarily a parasympathetic ganglion, although it has rich parasympathetic (preganglionic axons and postganglionic cell bodies and axons) and sympathetic (postganglionic axons) elements. The parasympathetic preganglionic cell bodies originate in the pons from the superior salivatory nucleus (SSN) of the facial nerve.
The efferent fibers of the SSN travel in the nervus intermedius and split at the geniculate ganglion unto the greater petrosal nerve and chorda tympani nerve. The first order preganglionic parasympathetic neurons in the greater petrosal nerve are joined by the postganglionic sympathetic fibers from the deep petrosal nerve to form the nerve to the pterygoid canal (vidian nerve). The preganglionic parasympathetic neurons then synapse with the second-order parasympathetic neuronal cell bodies located in the SPG. Therefore, the only cell bodies located within the SPG are those of the second-order postganglionic parasympathetic neurons.8 This may elucidate the clinical observation that patients after SPG radiofrequency ablationor neurostimulation may experience improvement of the autonomic parasympathetic symptoms either before or even without improvement of the headache pain symptoms.9 10
The activation of the parasympathetic outflow from the SPG leads to dilation of blood vessels, stimulation of lacrimal glands and trigeminal nerve endings. This results in lacrimation, redness of the eyes and nasal congestion, meningeal vasodilatation, neurogenic inflammation sensitizing the meningeal nociceptor and increased regional cerebral blood flow.11 12Accordingly, a useful biomarker for effective SPG parasympathetic block would be decreased regional cerebral blood flow or eye dryness.
The sympathetic cell bodies projecting to the SPG stem from the upper thoracic spinal cord. The first-order preganglionic sympathetic neurons then ascend through the cervical sympathetic chain to synapse primarily in the superior cervical ganglion. The postganglionic second-order sympathetic neurons form the carotid plexus and reach the pterygoid canal through the deep petrosal nerve where it joins the greater petrosal nerve, forming the vidian nerve. Postganglionic sympathetic fibers pass through the SPG without synapsing to innervate mainly the blood vessels (figure 1).
Anatomical illustration of the pterygopalatine fossa demonstrating the complex innervations within the fossa. Courtesy of Narouze.
PPF topographic anatomy
Pterygopalatine fossa (PPF) is a small upside-down pyramidal space, approximately 2 cm high and 1 cm wide. It is located posterior to the maxillary sinus and in front of the pterygoid process of the sphenoid bone. Medially, it is separated from the nose by the perpendicular plate of the palatine bone and communicate with the nasal cavity through the SPF located between the orbital and the sphenoidal process of the palatine bone. Laterally, the PPF opens into the infratemporal fossa through the pterygomaxillary fissure (PMF). Posteriorly, the PPF communicates with the middle cranial fossa through the foramen rotundum and the foramen lacerum via the pterygoid canal, and to the nasopharynx through the palatovaginal canal. Superiorly, the PPF connects to the orbit through the medial part of the inferior orbital fissure. Inferiorly, the PPF extends to the roof of the oral cavity through the greater palatine canal (figures 2 and 3).
Anatomy of the pterygopalatine fossa and its openings. Courtesy of Narouze.
Illustration of the openings of the pterygopalatine fossa and their contents. Courtesy of Narouze. SPG, sphenopalatine ganglion.
The PPF contains the maxillary nerve and branches (infraorbital nerve superiorly and the palatine nerves inferiorly), the SPG with afferent and efferent branches (vidian nerve, nasal and pharyngeal nerves), the maxillary artery and emissary veins. These PPF contents are located within an adipose tissue matrix13–15 (tables 1 and 2).
Pterygopalatine fossa (PPF) boundaries
The pterygopalatine fossa foramina, contents, connections and different approaches
Clinical anatomy relevant to SPG block
Traditionally, it was thought that the SPG is located directly under the nasal mucosa. Sluder projected the distance to be as small as 1 mm, although he conceded that there are significant inconsistencies and the SPG may be situated up to 9 mm from the SPF.16 17
Crespi and colleages’ findings challenge the assumption that the intranasal LA administration close to the SPF can passively diffuse to block the SPG. They examined 40 SPG in 20 patients with fused MRI/CT images and reported that the mean distance from the SPG to the closest point of the nasal mucosa covering the SPF was 6.77 mm (SD 1.75; range 4.00–11.60). Although the SPF connects the nasal cavity to the PPF, nasal endoscopy revealed that the foramen itself does not seem to be an open channel as it is packed with neurovascular structures in connective tissue and is covered by nasal mucosa.17
Another cadaveric anatomical report on 70 SPG found considerable individual variabilities in the structure and topography of the SPG. The SPG size was relatively stable at 3–5 mm, while its position within the PPF was quite variable. The SPG was surrounded by adipose tissue and located 3–4 mm and 10 mm from the nasal mucosa in approximately 50% and 30% of cases respectively (figure 4). In few cases, the SPG was located within the vidian canal, lending the SPG to be faraway and unreachable by intranasal LA.18
Axial CT images through the pterygopalatine fossa. The yellow crescent is the sphenopalatine ganglion (SPG). The white interrupted line is the distance from the closest point of the nasal mucosa to the SPG with a range of 4–12 mm. In this particular case, it is approximately 8 mm. The red line is the sphenopalatine foramen transverse diameter which is approximately 5 mm. The white bracket is the transverse diameter of the pterygo-maxillary fissure opening into the infratemporal fossa. The blue drops represent the local anesthetic installed into the nose. Courtesy of Narouze.
There is also marked variability regarding the size of the SPF in the literature. Prades et al examined 12 skulls and reported SPF mean height of 6.1 mm (range 5.2–6.8 mm) and mean width of 2.5 mm (range 2.4–2.5 mm).19 On the other hand, another morphometric CT study in 100 patients revealed that the transverse diameter of SPF is 3.5–7.8 (mean±SD: 5±0.9) in males and 3.2–5.6 (mean±SD: 4.4±0.6) in females.20
Gibelli and colleages assessed the height and volume of the PPF based on 3-D segmentation on head CT-scan in 100 patients. The mean PPF height was 24.1±3.5 mm in males and 22.8±3.4 mm in females, whereas the mean PPF volume was 0.930±0.181 mL in males and 0.817±0.157 mL in females21 (table 3).
Common pterygopalatine fossa (PPF) measures related to the nasal approach
Approaches to the pterygopalatine fossa (PPF)
As the PPF has seven openings, theoretically the fossa can be accessed through any of these foramina. However, the clinically feasible non-invasive approaches are listed in table 2.
1- Sphenopalatine foramen (SPF) approach
Topical intranasal LA application ‘blind alleged block’
Sluder—in 1908—first proposed blocking the SPG using topical cocaine applied transnasally to the posterior wall of the nasopharynx in the region of the middle turbinate. It was thought that the SPG is located directly under the nasal mucosa and LA can diffuse across the mucosa and SPF to reach the PPF and block the SPG (see above).22 Different variations of this approach were described, including the utilization of specially designed catheters.23
Transnasal endoscopic approach ‘guided actual block’
Nasal endoscope is used to locate the nasal mucus membrane immediately behind and over the middle turbinate tail. Then after, a needle is inserted into the inferior portion of the SPFwhile avoiding the sphenopalatine artery.24
2- Greater palatine canal approach
Transoral approach
This approach is usually used by dentists with the aim to block the palatine nerves. The PPF is accessed transorally by placing a small 27 G needle inside the greater palatine foramen at the roof of the mouth.25
3- Pterygomaxillary fissure (PMF) approach
Percutaneous infrazygomatic approach
This is the approach typically used for neuromodulation and neuroablation techniques. The needle placement is guided by either fluoroscopy or CT guidance.8 26 The infrazygomatic approach could be either anterior to the mandible or through the coronoid notch of the mandible.8
4- Transoral surgical approach
This approach is used to implant of the mini SPG neurostimulator. This new minimally invasive transoral approach uses an incision in the gingival mucosa above the maxillary molars. The implant is surgically placed with the electrode tip close to the SPG inside the PPF.27
‘Presumed’ and ‘proposed’ mechanisms of action of intranasal Lidocaine
Initial reports of randomized controlled trials (RCTs) of intranasal LA administration for headache management date back to the 1990s.28 A recent meta-analysis of six RCTs concluded that intranasal lidocaine is a useful tool in patients with acute migraine.29 Of note, currently there are three negative RCTs.30–32
The proposed mechanism of action is that LA administered intranasally in the proximity of the SPF can diffuse from the intranasal cavity to reach and block the SPG, as historically Sluder reported in 1909 that the SPG is about 1 mm deep to the nasal mucosa in the area of the SPF.16 Although Sluder acknowledged that there are significant inconsistencies and the SPG may be situated up to 9 mm from the SPF.16
Most of the LA applied nasally will descent to the pharynx and swallowed. This is evident by the common complaints of bitter taste and mouth numbness.17 33 34 Logically, the remaining few drops of LA will not be sufficient enough to diffuse through the nasal mucosa, SPF and PPF adipose tissue to reach the SPG in sufficient concentration and volume to produce effective block.
Possible explanations of the observed effect of intranasal LA might be due to systemic absorption rather than SPG block.35 36 Berger et al reported that topical nasal LA may relieve low back pain and he could not explain this on anatomical or physiological basis and this raised the question regarding systemic LA effects.36 Topical anesthesia is another plausible mechanism. Intranasal local anesthesia is a standard technique utilized in transnasal surgery as it blocks first and second trigeminal nerve endings in the nasal mucosa.37 This also explains why intranasal lidocaine in headache patients is most effective for pain in the orbital and nasal areas.38 Moreover, one should not exclude possible placebo effect. At least in one RCT, the effect of intranasal bupivacaine was similar to intranasal saline administration.32
In conclusion, intranasal LA application is not a true SPG block and the reported headache relief could be explained by systemic absorption of LA or a placebo effect. I propose another theory that nasal mucosal irritation may lead to reflex cerebral vasoconstriction. However, this needs to be explored, investigated and validated.
References
Footnotes
Twitter @NarouzeMD
Contributors SN is the only author and this is his original work.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Patient consent for publication Not required.
Provenance and peer review Not commissioned; externally peer reviewed.
Data availability statement All data relevant to the study are included in the article.