Diagnosis and Management of Lingual Nerve Injuries.

Injury to the lingual nerve is a well-recognized risk associated with certain routine dental and oral surgical procedures. The assessment and management of a patient with a traumatic lingual nerve neuropathy requires a logical and stepwise approach. The proper application and interpretation of the various neurosensory tests and maneuvers is critical to establishing an accurate diagnosis. The implementation of a surgical or nonsurgical treatment strategy is based not only on the established diagnosis, but also a multitude of variables including patient age, timing and nature of the injury, and the emotional or psychological impact.

Neuromodulation of the lingual nerve: a novel technique.

Acute injury of the trigeminal nerve or its branches can result in posttraumatic trigeminal neuropathy (PTTN). Affected patients suffer from chronic debilitating symptoms long after they have recovered from the inciting trauma. Symptoms vary but usually consist of paresthesia, allodynia, dysesthesia, hyperalgesia, or a combination of these symptoms. PTTN of the trigeminal nerve can result from a variety of traumas, including iatrogenic injury from various dental and maxillofacial procedures. Treatments include medications, pulsed radiofrequency modulation, and microsurgical repair. Although trigeminal nerve stimulation has been reported for trigeminal neuropathy, V3 implantation is often avoided because of an elevated migration risk secondary to mandibular motion, and lingual nerve implantation has not been documented. Here, the authors report on a patient who suffered from refractory PTTN despite multiple alternative treatments. He elected to undergo novel placement of a lingual nerve stimulator for neuromodulation therapy. To the best of the authors' knowledge, this is the first documented case of lingual nerve stimulator implantation for lingual neuropathy, a technique for potentially reducing the risk of electrode migration.

Functional regeneration of the transected recurrent laryngeal nerve using a collagen scaffold loaded with laminin and laminin-binding BDNF and GDNF.

Recurrent laryngeal nerve (RLN) injury remains a challenge due to the lack of effective treatments. In this study, we established a new drug delivery system consisting of a tube of Heal-All Oral Cavity Repair Membrane loaded with laminin and neurotrophic factors and tested its ability to promote functional recovery following RLN injury. We created recombinant fusion proteins consisting of brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF) fused to laminin-binding domains (LBDs) in order to prevent neurotrophin diffusion. LBD-BDNF, LBD-GDNF, and laminin were injected into a collagen tube that was fitted to the ends of the transected RLN in rats. Functional recovery was assessed 4, 8, and 12 weeks after injury. Although vocal fold movement was not restored until 12 weeks after injury, animals treated with the collagen tube loaded with laminin, LBD-BDNF and LBD-GDNF showed improved recovery in vocalisation, arytenoid cartilage angles, compound muscle action potentials and regenerated fibre area compared to animals treated by autologous nerve grafting (p < 0.05). These results demonstrate the drug delivery system induced nerve regeneration following RLN transection that was superior to that induced by autologus nerve grafting. It may have potential applications in nerve regeneration of RLN transection injury.

When to refer a patient with a nerve injury to a specialist.

BACKGROUND: Nerve injury is a known and accepted risk of many oral surgical and dental procedures. Such injuries may occur despite the practitioner's providing the best of care. Taking proactive measures during evaluation and surgery may reduce the incidence of nerve injury. RESULTS: Injuries to the peripheral branches of the trigeminal nerve can cause unfavorable effects on orofacial sensation and related functions such as eating, drinking, washing, speaking, shaving and kissing. CONCLUSIONS: When nerve injuries secondary to dental or oral surgery procedures fail to resolve promptly and the resulting dysesthesia is unacceptable to the patient, timely treatment gives the patient the best chance of a favorable outcome. Treatment may involve surgical exploration and repair of the injured nerve. PRACTICAL IMPLICATIONS: Recognition of and prompt referral for nerve injuries give the patient the best chance of achieving improvement or recovery of sensory function in the distribution of the injured nerve.

Managing iatrogenic trigeminal nerve injury: a case series and review of the literature.

This study describes the management of 216 patients with post-traumatic iatrogenic lingual nerve injuries (LNIs; n=93) and inferior alveolar nerve injuries (IANI; n=123). At initial consultation, 6% IANI and 2% LNI patients had undergone significant resolution requiring no further reviews. Reassurance and counselling was adequate management for 51% IANI and 55% LNI patients. Systemic or topical medication was offered as pain relief to 5% of patients. Additional cognitive behaviour therapy (CBT) was offered to 8% of patients. Topical 5% lidocaine patches reduced pain and allodynia in 7% of IANI patients, most often used without any other form of management. A small percentage of IANI patients (4%) received a combination of therapies involving CBT, surgery, medication and 5% lidocaine patches. Exploratory surgery improved symptoms and reduced neuropathic area in 18 LNI and 15 IANI patients resulting in improved quality of life. In conclusion, the authors suggest a more diverse and perhaps holistic strategy for management of patients with iatrogenic trigeminal nerve injuries and recommend pragmatic assessment criteria for measurement of treatment success in these patients.

The effect of a monoclonal antibody to calcitonin-gene related peptide (CGRP) on injury-induced ectopic discharge following lingual nerve injury.

The development of ectopic neural discharge at a site of peripheral nerve injury is thought to contribute to the initiation of sensory disturbances and pain. We have previously shown that this discharge can be initiated or increased by the neuropeptide calcitonin gene-related peptide (CGRP). We have now studied a potential therapeutic approach to reducing the discharge by evaluating the effect of a systemically administered monoclonal antibody to CGRP on injury-induced activity in the lingual nerve. In 16 anaesthetised adult ferrets the left lingual nerve was sectioned. One day after the injury, the animals received a subcutaneous injection of either a monoclonal antibody to CGRP or a vehicle control. Three days after the injury, under a second anaesthetic, single-unit electrophysiological recordings were made from central to the injury site (469 and 391 units were analysed in antibody and vehicle groups, respectively), and the proportion of units that were spontaneously active was determined. In the vehicle-treated animals 6.4±2.7 [SEM]% of the units were spontaneously active, with conduction velocities of 8.8-40.8m/s and discharge frequencies of 0.03-2.7Hz. In the monoclonal antibody-treated animals 5.7±2.0% of the units were spontaneously active, with conduction velocities of 13.9-38.8m/s and discharge frequencies of 0.07-1.8Hz. There was no significant difference between these two groups (for spontaneous activity and conduction velocity: p>0.05, Student's t-test; for discharge frequency: p>0.05, Mann-Whitney test), suggesting that the spontaneous activity initiated by a nerve injury cannot be modulated by administration of a monoclonal antibody to CGRP.