Transient glossopharyngeal nerve palsy due to mandibular nerve block
- 1 Department of Physiotherapy, Laboratory of Neuromuscular and Cardiovascular Study of Motion, University of West Attica, Egaleo, Greece
- 2 School of Dentistry, University of Athens, Athens, Greece
- Correspondence to Dr Marianna Papadopoulou; marpapgr@yahoo.co.uk
Abstract
Local anaesthesia in dental procedures is considered safe. Few cases of neurological complication have been reported, most of which involve the lingual or inferior alveolar nerve. We report a case of a woman in her late 40s who 30 min after administration of local anaesthetic in the right pterygomandibular space (articaine and mepivacaine) developed nasal speech and numbness in the area around external auditory meatus. Uvula was deviated to the left. No facial palsy or diplopia were observed. The symptoms subsided gradually after 3 hours. Clinical symptoms were attributed to glossopharyngeal nerve palsy. Glossopharyngeal nerve palsy after mandibular nerve block has never been reported before. Reporting cases of neurological complications of a very common and generally safe procedure help in increasing the awareness of potential risks considering the anatomical complexity and variability of the orofacial area.
Background
Local anaesthesia is a standard procedure in everyday dental practice in order to attain analgesia. Although it is considered generally safe, complications do occur. Reporting potential risks associated with oral injections and recognising the likelihood of complications can help reduce the incidence of such side effects.1 Systemic complications are attributed to accidental intravascular injection but are considered rare. Local complications are either due to direct nerve damage or to neurotoxicity of the local anaesthetic. Direct nerve trauma is thought to be caused when needle barb ruptures connective tissues and damages nerve fibres or if intraneural haematoma develops due to trauma of vasa nervorum. In both cases, although complete nerve damage (neurotmesis) is rarely reported, recovery might be delayed until remyelination (in cases of neurapraxia) and/or axonal regeneration (in cases of axonotmesis) is completed. In most cases, where neurological symptoms occur but only last for couple of hours, chemical damage to the nerve seems to be a more plausible explanation.
It is estimated that 1 in 20 000–850 000 patients will present nerve involvement after mandibular nerve block, with articaine been associated in more cases relatively to other agents.2 In most published papers, lingual nerve trauma accounts for 70% of cases, and this is attributed to its very superficial position under the mucosa, near the site of needle penetration for mandibular nerve block, resulting in numbness in the tongue. In the rest cases of sensory sequelae, inferior alveolar, mental and rarely chordi tympani nerves are involved.3 Other less common nerve injuries have been reported, such as facial nerve palsy, either of immediate or late onset, probably because of anatomic variant of the nerve, transient amaurosis, an almost terrifying complication due to infusion of the anaesthetic drug in the central retina artery through retrograde flow in the maxillary artery, diplopia attributed to flow of the drug in the cavernous sinus and paralysis of nerves III, IV and VI, Horner’s syndrome due to blockade of stellate ganglion and even deafness due to cochlear nerve dysfunction.4 It is generally agreed that the higher the concentration of anaesthetic, the higher the risk of neurological complications.5
Case presentation
We report a case of pharyngeal muscles palsy that occurred about 30 min after administering local anaesthetic for right mandibular nerve block for routine dental procedure (scaling and root planing for periodontitis treatment). The patient was a middle aged woman, a doctor by profession, with a free medical history and not mentioning any allergies. Articaine 4% plus epinephrine were initially administered (40 mg/mL plus 1:100000, respectively, one ampoule of 1.7 mL) with a needle 0.30×25 mm 30G. After 5–10 min, because of inadequately achieved anaesthesia in tongue, a further administration of mepivacaine 3% (30 mg/mL one ampoule of 1.8 mL) was infused in the same spot as the first one. After 5 min, anaesthesia in the distribution of inferior alveolar nerve was achieved, but not in the tongue (lingual nerve). The dental procedures were completed with slight annoyance, and the patient left the dental office. Half an hour later, the patient felt difficulty in swallowing saliva and her speech became nasal. Self-inspection revealed uvula deviation to the left. She felt numbness in front of the helix and tragus but never felt numbness in tongue. No facial palsy or diplopia were observed.
Investigations
The patient, being a doctor, was inspecting herself and was in constant contact with the dentist. She avoided drinking or eating anything to protect the airways. The symptoms lasted for about 3 hours and gradually subsided without any special treatment.
Differential diagnosis
This is the first case of transient palsy of pharyngeal musculature occurring as a complication of mandibular nerve block in the pterygomandibular space. It is questionable which nerve was injured. The fact that numbness occurred in the proximal area of the ear could implicate almost four cranial nerves: trigeminal, facial, glossopharyngeal nerve (GPN) and vagus nerve (VN). Since no facial palsy was observed, VII injury was ruled out. Mandibular nerve, the third branch of trigeminal nerve, may have accounted for numbness in the area, but it is almost impossible to have produced uvula deviation due tensor palatine muscle palsy only. Furthermore, the fact that no numbness occurred in tongue implies that finally lingual nerve was not affected by the local anaesthetic. Therefore, numbness around the ear and uvula deviation should probably be attributed to VN and GPN.
Outcome and follow-up
Eventually, as it happens in most cases of nerve palsies after local anaesthesia, symptoms subsided without special treatment and without any residues.
Discussion
The muscles of the pharynx are innervated by the pharyngeal plexus which consists of fibres from cranial nerves GPN and VN. The exact innervation of the pharyngeal wall is unclear and debated. It is commonly accepted that motor branches of VN innervate almost all pharyngeal muscles, whereas GPN serves mainly as a sensory nerve of pharyngeal area. It is assumed that motor roots of the GPN supply both the stylopharyngeus and the lateral portion of the superior constrictor muscle. In 8% of people, isolated GPN palsy can present with nasal regurgitation due to common motor nerve supply to the levator veli palatini instead of receiving motor innervation from VN.6 The clinical picture of the patient, nasal speech due to soft palate paralysis and numbness in external ear area could not easily attributed to VN injury. Injury of VN would have resulted in symptoms from inhibition of parasympathetic fibres, giving rise to tachycardia and hypertension, and moreover palsy of laryngeal muscles, symptoms that were not observed. Bearing in mind the above anatomical considerations regarding distribution of motor and sensory fibres of cranial nerves, GPN injury seems the most plausible explanation of the clinical picture.
GPN exits the skull via the jugular foramen along with VN and spinal accessory nerves and descends forward and inferiorly passes in between the internal jugular vein and the internal carotid artery (ICA). It descends anterior to the ICA and courses medially behind the styloid process while continuing to its main branches aiming to the root of the tongue. The nerve passes between the stylopharyngeus muscle and the styloglossus muscle, enters the prestyloid space and ends its course beneath the mucosa of the posterior one-third of the tongue, medially to the styloglossus muscle, dividing into its terminal lingual branches which are sensory and afferent gustatory and innervate the mucosa of the posterior one-third of the tongue (figure 1).
Illustration of XI (glossopharyngeal) course and its anatomic relations to nerves V (trigeminal), VII (facial), X (vagus) and XI (accessory) and ICA (internal carotid artery and IJV (internal jugular vein vessels. The blue circle indicates the needle insertion site behind the lower second molar tooth. It is suggested that drug diffusion reached glossopharyngeal nerve (GPN) and inferior alveolar nerve but failed to reach lingual nerve.

In the case of mandibular nerve block, GPN could have been damaged at the styloid process located posterolaterally or at the pharyngeal plexus in the posterior pharyngeal wall in the carotid triangle. The carotid triangle may be reached by an intraoral approach via the submandibular triangle, the floor of which is the mylohyoid muscle anteriorly and the hyoglossus muscle posteriorly. Since symptoms lasted for only a couple of hours, direct nerve injury is not a very possible explanation. Most probably, insertion of the needle behind the lower second molar tooth led to a drug diffusion in the parapharyngeal space that then spread through loose facial clefts in the carotid triangle where it reached GPN.7
Neurological complications related to local anaesthesia are rare, but since it is a common practice, dentists might confront such events in their everyday practice. Most commonly, neurological complications are sensory, such as transient or more persistent dysaesthesia or even anaesthesia in the distribution of lingual or inferior alveolar nerve. Motor complications occur quite seldom but are more terrifying for the patient and the doctor. To the best of our knowledge, this is the first case of GPN palsy after mandibular nerve block in a standard dental procedure with a good outcome. Reporting cases of neurological complications help to increase the awareness of potential risks, considering the anatomical complexity and variability of the orofacial area.
Patient’s perspective
It was a terrifying situation. Soon after I left the dentist’s office, I realised that my speech has changed and became nasal. In addition, it was difficult to swallow my saliva. I could clearly see in the mirror my uvula deviated to the left and I immediately understood that a nerve palsy had occurred, but at that moment, I could not figure out which nerve was affected. I immediately called the dentist and described what had happened. It was even more frightening to hear that this complication has never happened to him before. Being a doctor myself made thing more complicated, as I feared of further paralysis and the possibility of airway closure. Fortunately, after a few hours of agony, the palsy begun to subside. It was one of the worst experiences I have ever had although I understand the benign nature of the complication.
Learning points
-
Local anaesthesia in dental practice is a standard procedure and is considered generally safe.
-
Complications after local anaesthesia are transient and attributed either to direct nerve damage or to neurotoxicity.
-
The higher the concentration of anaesthetic, the higher the risk of neurological complications.
-
Most commonly reported complication is lingual nerve injury resulting in numbness of the tongue.
-
Diffusion of anaesthetic into the parapharyngeal space can affect glossopharyngeal nerve and lead to unusual clinical pictures.
Ethics statements
Patient consent for publication
Footnotes
-
Contributors MP conceptualisation and revising. MP and SA drafting of the manuscript.
-
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.
-
Case reports provide a valuable learning resource for the scientific community and can indicate areas of interest for future research. They should not be used in isolation to guide treatment choices or public health policy.
-
Competing interests None declared.
-
Provenance and peer review Not commissioned; externally peer reviewed.
- © BMJ Publishing Group Limited 2022. No commercial re-use. See rights and permissions. Published by BMJ.
References
Use of this content is subject to our disclaimer