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Lingual nerve injury is a common complication following dental and medical procedures. The clinical presentation of lingual nerve injury, its epidemiology, predisposing factors, and anatomy are explored in an attempt to identify those patients at risk for developing neuropathic pain. Nonsurgical and surgical therapies also are discussed.
Lingual nerve injury is an uncommon complication of laryngoscopy. We report a case of isolated unilateral lingual nerve injury that occurred during suspension microlaryngoscopy. The injury was transient, with complete return of sensation within 3 months after surgery. Several mechanisms have been proposed to explain the occurrence of lingual nerve injury during laryngoscopy, including direct compression of the nerve caused by the laryngoscope, stretching of the nerve caused by cricoid pressure or instrumentation, and compression of the nerve between the medial and lateral pterygoid caused by manipulation of the mandible. The precise mechanism of injury in this case was not obvious, but stretching of the lingual nerve caused by pressure of the suspended laryngoscope on the tongue or retrolingual region was likely. The transient nature of the injury and the rapid return of the nerve to baseline function in this case are consistent with a neurapraxic injury.
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Injuries to the lingual nerve remain a relatively uncommon event. However, given the frequency of surgical procedures in this anatomic region, it is likely that every oral and maxillofacial surgeon will be required to manage such an injury. When spontaneous recovery of lingual sensation is absent, microsurgical reconstruction can predictably achieve improved sensation in a majority of patients provided that such injuries are properly assessed and treated early. The quality of the sensory improvement is related to the age of the patient, the timing of surgery, the extent of the neural injury, and the quality of the repair.
The aim of this study was to investigate risk factors for temporary and permanent lingual nerve injury after extraction of mandibular third molars. It was based on a 4-year prospective study of 2134 consecutive mandibular third molar operations in 1384 consecutive day case patients. During the study period (1994-1998) data were collected prospectively on patient, dental and surgical factors and correlated with lingual nerve injury using Student's t test, xi(2) and multiple logistic regression analysis. The incidence of temporary and permanent lingual nerve injury was 1 and 0.3%, respectively, per tooth. Factors that predicted temporary and permanent lingual nerve injury by univariate analysis were age, depth of application, difficulty of operation, surgeon and surgical technique used. Independent risk factors identified by multivariate analysis for temporary lingual nerve injury were perforation of the lingual plate, exposure of the nerve and increased difficulty of operation. The predictors for permanent lingual nerve injury in order of importance were perforation of the lingual plate, surgeon, increased difficulty of operation, exposure of the nerve and increased age of the patient. Surgical factors are the main contributors to lingual nerve injury during third molar extraction, but patient and dental factors are also involved.
A method for assessing lingual sensation is described, comprising sensory testing, using touch and moving two-point discrimination and patient subjective reporting. The clinical application is seen to be the evaluation of lingual nerve injury consequent upon lower third molar surgery. Using this method it is considered possible to identify many of those patients unlikely to make full spontaneous recovery at the stage of 3 months following injury, with a view to achieving an earlier timing of surgical repair than that which prevails at present.
A lingual nerve injury is an infrequent but unpleasant complication of the removal of lower third molars. The nerve stays at risk even with a correct technique. The classifications of nerve injuries of Seddon and Sunderland give insight in the complexity and give guidelines for prognosis and treatment. Degeneration and regeneration as in other peripheral nerves occur also here and knowledge of these phenomena is crucial for the success of the microsurgical repair. Confronted with the problem, an attempt to a correct evaluation of the extent of the injury should be done, and transfer to a specialist is necessary when the dysesthesia is still persistent after more than 2 months.
INTRODUCTION: Lingual nerve injury is one of the most important complications after removal of a lower third molar. CASE REPORT: We report two cases of this complication in our experience. In the first case, lingual nerve injury was repaired immediately and the patient recovered total tongue sensitivity. In the second case, lingual nerve exploration was not undertaken and the patient developed complete tongue anesthesia. DISCUSSION: Opinions are quite different about the delay before exploration of an injured lingual nerve. However, absence of sensory improvement incited us to undertake surgical exploration of the nerve. Due to the degenerative lesion of the damaged nerve, timing of repair before three months seems preferable. In young patients, early repair, and good quality nerve suture without tissue loss improve sensitive recovery of the tongue.
We present a case of lingual nerve injury that was associated with use of the ProSeal laryngeal mask airway during shoulder replacement in a 61-yr-old male. We also review other cases of cranial nerve injury, most of which were associated with use of the classic laryngeal mask airway. In principle, the frequency of cranial nerve injuries can be reduced by avoiding insertion trauma, using appropriate sizes, minimizing cuff volume, and early identification and correction of malposition.
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The extent of reflex inhibition of masseteric electromyographic activity, after an electrical stimulus applied to lingual mucosa, was used as a test of the ability of the lingual nerve to conduct nerve impulses and this was compared with the results of standard clinical tests. Two groups of subjects were assessed: healthy subjects (n=10) and patients with lingual nerve injuries (n=17). The patients were tested 8-9 weeks after their injury and retested 6 months later when they were retrospectively allocated to either a temporary injury or a permanent injury group. The group measure of reflex inhibition after stimulation of the tongue on the opposite side to the injury was no different from the same measure in controls, whereas two-point discrimination did differ. Group measures of inhibition and of subjective function after stimulation on the side of the injury were significantly different from controls whereas light touch and two-point discrimination were not. There was good agreement between quantified masseteric inhibition and subjective function, but it was not possible at 8-9 weeks after the injury to differentiate between those that would recover and those that would be permanent.
Investigations into the aetiology of nerve injury-induced dysaesthesia have revealed the development of spontaneous and mechanically-induced activity from damaged axons. Pharmacological manipulation of this activity could provide a method of treatment for this intractable condition. This study has investigated the effect of a corticosteroid applied to the injury site, as these agents are known to reduce inflammation and scarring. In 24 anaesthetised adult ferrets the left lingual nerve was sectioned and the animals allowed to recover. In eight of these animals the nerve was re-exposed under anaesthesia after 1 month and 100 microl of corticosteroid (triamcinolone hexacetonide, 20 mg/ml) was injected into and around the injury site. In eight others, 100 microl of the steroid carrier was injected, and the eight remaining animals were used as controls. In terminal experiments under general anaesthesia, 3 months after the initial injury, electrophysiological recordings were made from axons in fine filaments dissected from the nerve central to both the injury site and junction with the chorda tympani nerve. Spontaneous activity (SA) was found in approximately 13% of units in control animals, 12% following the application of steroid, and 14% in the carrier group. Mechanically-induced activity at the injury site was found in approximately 13% of units in controls, significantly fewer after the application of steroid 4% (P<0.001) and 12% in the carrier group. These data suggest that local application of the corticosteroid triamcinolone hexacetonide could reduce the level of mechanically-induced, but not spontaneous, dysaesthesia following lingual nerve injury.
The sagittal ramus osteotomy of the mandible is the most frequently performed orthognathic surgical procedure. Stabilization of the osteotomy may be accomplished by rigid internal or wire fixation. This article illustrates lingual nerve injury following a bilateral sagittal ramus osteotomy of the mandible and fixation with a superior border wire. The etiology and surgical management of this injury are described.
The recovery of fibres in the chorda tympani and lingual nerves has been investigated in cats following nerve injury by recording the receptor properties of gustatory, thermosensitive and mechanosensitive units and the return of vasomotor and secretomotor responses. The combined trunk of the chorda tympani and lingual nerves was either crushed (4 animals) or sectioned (3 animals) unilaterally and recovery allowed for 12 weeks. After nerve crush, integrated whole nerve activity recorded from the chorda tympani during stimulation of the tongue with gustatory or thermal stimuli revealed a response profile which was similar to controls. After nerve section little or no activity could be recorded. Recordings made from 52 single units in the chorda tympani after nerve crush revealed that the proportions of gustatory, thermosensitive and mechanosensitive units were similar to those of controls. The units had slower conduction velocities, responded less vigorously and to a narrower range of stimuli. Recordings made from 46 units in the chorda tympani after nerve section revealed very few gustatory or thermosensitive units, the majority were purely mechanosensitive and the decrease in conduction velocity was greater than after nerve crush. Electrical stimulation of efferent vasodilator fibres in both the chorda tympani and lingual nerves, evoked a temperature rise on the dorsal surface of the tongue. This effect was completely restored after nerve crush but was significantly smaller after nerve section. The flow rate of saliva from the submandibular salivary gland was not significantly changed by nerve crush but was significantly smaller after nerve section. There was no evidence for functional reinnervation of gustatory or secretomotor terminals by inappropriate fibre types.
We report a patient who presented for elective myomectomy. Laryngoscopy and endotracheal intubation were achieved smoothly without unduly force. An oropharyngeal airway was inserted after endotracheal intubation for biting and was left in the oral cavity until the end of surgery. Two days after surgery, the patient complained of numbness on the right side of her tongue. Neurological examination revealed an area of hypesthesia about 1 cm in diameter on the right side of the tongue tip. The motor function, taste perception, and speech articulation were all intact. A right lingual nerve lesion with terminal branch involvement was diagnosed. The patient was then reassured and discharged home. At the 4-week follow-up, spontaneous resolution occurred. After reviewing the history, we speculated that the mechanism of nerve injury in this case was a direct compression of the tongue tip by the oropharyngeal airway. This is the first report of lingual nerve injury caused by improper placement of the oropharyngeal airway. We recommend careful manipulation in the use of the oropharyngeal airway and vigilant surveillance being undertaken when an oropharyngeal airway is left in place for a prolonged period.
Lingual nerve damage subsequent to lower wisdom tooth removal affects a small number of patients, sometimes producing permanent sensory loss or impairment. A number of surgical techniques have been described which are associated with low incidences of this distressing post-operative complication. When a technique is adopted by an individual clinician then a personal audit may be prudent to establish how effective it is in relation to established nerve injury rates. This audit looks at a technique involving the minimal interference of lingual soft tissues during lower wisdom tooth removal in a high street practice situation for patients having mild to moderate impacted wisdom teeth removed under local anaesthetic. It was concluded that the technique employed was associated with a low incidence of lingual nerve trauma, comparable with that reported elsewhere.
PURPOSE: It has been suggested that different etiologies of lingual nerve damage in the third molar area will produce a different clinical and histologic appearance in the nerve. If the clinical and histologic pictures were different, it could result in different treatments being recommended. MATERIALS AND METHODS: Eight preserved cadavers (16 lingual nerves) were used for this study. As far as possible, the nerves were left in situ and damaged in a way that could be envisaged during third molar surgery. In each case, the damaged sections of nerve were photographed, resected, embedded in paraffin wax, sectioned in 5 mum sections, stained with hematoxylin-eosin, and examined histologically. RESULTS: The scalpel clinically produced a clean wound with sharply defined edges; this was confirmed histologically with minimal disruption to the fascicles. The 702 fissure bur produced a ragged stretch-type injury clinically, and histologically this was confirmed with an irregular-edged border to the lesion and stretching and internal damage to the fascicles immediately adjacent to the wound. The crush injury clinically caused considerable apparent damage to the nerve, which was confirmed histologically with crushing and disruption of the fascicles and reduction to approximately 25% of their preinjury thickness. The stretch injury clinically showed no damage, but histologically showed irregular internal disruption of the fascicles over the whole area subject to stretching movements. CONCLUSION: It does appear that different modalities in nerve injury produce a different type of injury both clinically and histologically. This information has implications for both natural clinical recovery and the indications for surgical intervention. Clinical recovery may occur best with close approximation of a sharp scalpel-type wound or excision of a crushed area of nerve with reapproximation of the nerve endings, but a ragged wound caused by a fissure bur may require excision back to healthy nerve with subsequent reapproximation, whereas with the stretching injury it may be difficult to ascertain the edges and limits of the wound, and difficult to repair, and it may be most appropriate to rely on a natural healing process for the best results.