The Management of Nerve Injuries

Trigeminal nerve injuries are common and can be extremely distressing for the patient. The inferior alveolar and lingual nerves are most frequently damaged during lower third molar removal, but may also suffer injury during surgery for facial deformity or as a result of facial fractures. Although the majority of patients regain normal sensation within a few weeks or months, a proportion are left with abnormal sensation or pain, which can cause difficulty with speech and mastication, and is a frequent cause of litigation against the surgeon.

In the past, little was offered to these patients, either in terms of a clear prognosis or possible surgical intervention to improve the level of recovery. Now, as a result of our work, there is a scientific basis for the management of this problem. Our studies have answered a number of fundamental questions in the following areas:

Surgical intervention

Intervention is required in some circumstances, as nerve repair can improve recovery. We have shown that repair of a cut lingual nerve using epineurial sutures is more effective than entubulation and, if a damaged nerve segment has to be excised, repair by stretching the ends under slight tension is better than grafting. If a graft is essential, a frozen skeletal muscle autograft is as good as a sural nerve graft and avoids donor site morbidity.

Clinically, delay prior to lingual nerve repair is essential as, in the early stages after injury, it is not possible to distinguish between anaesthesia resulting from a crush injury (which will not require intervention) and that resulting from a section injury (which requires repair). This distinction can normally be made at approximately three months post-injury and, fortunately, our studies have shown that this delay has little effect on the outcome.

Our prospective, quantitative assessment of the outcome of lingual nerve repair has revealed that, although the outcome is variable, there is a highly significant improvement in the majority, and patients consider the surgery worthwhile.

Surgical repair of damaged lingual nerve

An operation to surgically repair a damaged lingual nerve, using the operating microscope.

Enhancing regeneration

We have shown that incorporation of growth factors at a site of nerve repair can preferentially enhance the regeneration of specific groups of nerve fibres. This suggests that future therapeutic enhancement of regeneration after peripheral nerve injury may require a combination of different growth factors, appropriate to the damaged nerve.

Scarring at a site of nerve repair is thought to impede the regeneration of damaged nerve fibres. Our recent studies have shown that anti-scarring agents (such as antibodies to TGFβ1 and 2) can be used to reduce this problem, and hopefully will result in enhanced regeneration.

Prevention of injury

The most important approach to nerve injuries is prevention. The incidence of lingual nerve injuries during third molar surgery in the UK is significantly higher than in other parts of Europe and in the USA. We have shown that this difference results from the UK method of elevation of a lingual flap and insertion of a Howarth´s periosteal elevator.

We undertook the first randomised controlled trial into the effect of this surgical technique, and found that avoidance of lingual flap retraction resulted in a significant reduction in lingual nerve injury. We concluded that, for the majority of cases, lingual retraction should be avoided. This has led to an evidence-based change in the recommended surgical technique taught in the UK, and has had a substantial impact on clinical practice.

Electron micrograph

An electron micrograph of human lingual nerve damaged during third molar removal, showing axonal exposure (arrowheads) and apposition (arrows) of unmyelinated nerve fibres.

Reducing injury-induced pain

At present, little can be offered to patients who develop the persistent painful condition of dysaesthesia after nerve injury, and understanding the aetiology of this disorder remains one of our key objectives.

We have undertaken a series of investigations on specimens of human lingual nerve tissue (obtained at the time of nerve repair) in an attempt to identify characteristics that are unique to those patients who have developed pain. This has shown that neuropeptides accumulate at the injury site and we think that this may be associated with the development of spontaneous activity and mechanical sensitivity in some damaged axons. Modifying the action of these neuropeptides could provide a pharmacological approach to treatment.

Ultrastructural studies on this human tissue have shown that both myelinated and unmyelinated fibres are smaller than normal and there is a significantly higher incidence of both axonal exposure and axonal apposition. These ultrastructural changes may account for some of the altered behaviour of the damaged nerve fibres, possibly leading to the development of pain.

In other studies we have found changes in other regulators of neuronal excitability, such as nitric oxide and specific sodium channel subtypes. These changes may also contribute to the development of abnormal activity from the damaged nerve fibres.

In pharmacological studies we have found that the application of corticosteroids to an injury site could decrease the pain evoked by mechanical stimulation of the damaged nerve fibres, and carbamazepine could reduce the spontaneous pain. We are undertaking clinical trials on the use of potential agents for the treatment of dysaesthesia.

Light micrograph

A light micrograph of human lingual nerve damaged during third molar removal, showing accumulation of sodium channel Na<sub>v</sub>1.7 within the damaged nerve fibres.


This area of research has been funded by grants from:

  • MRC
  • Wellcome Trust
  • Action Medical Research
  • Sir Jules Thorne Charitable Trust
  • GlaxoSmithKline
  • Pfizer

Key Staff

Names link through to personal profiles where available.

Key recent publications

Current management of damage to the inferior alveolar and lingual nerves as a result of removal of third molars. P P Robinson, A R Loescher, J M Yates and K G Smith. British Journal of Oral & Maxillofacial Surgery, 42; 285-292, 2004.

Peripheral mechanisms for the initiation of pain following trigeminal nerve injuries. P P Robinson, F M Boissonade, A R Loescher, K G Smith, J M Yates, et al J Orofacial Pain, 18; 287-292, 2004.

Close apposition and exposure of non-myelinated axons in traumatic neuromas of the human lingual nerve. A R Vora, A R Loescher, F M Boissonade & P P Robinson. J Peripheral Nervous System, 9; 200-208, 2004.

Ultrastructural characteristics of axons in traumatic neuromas of the human lingual nerve. A R Vora, A R Loescher, F M Boissonade & P P Robinson. J Orofacial Pain, 19; 22-33, 2005.

Nav1.7 sodium channel expression in human lingual nerve neuromas. E V Bird, F M Boissonade, P P Robinson. Archives of Oral Biology, 2007.

Inflammatory cell accumulation in traumatic neuromas of the human lingual nerve. A R Vora, S Bodell, K G Smith, A R Loescher, P P Robinson & F M Boissonade . Archives of Oral Biology, 52; 74-82, 2007.

Vanilloid receptor 1 (TRPV1) expression in human lingual nerve neuromas from patients with or without symptoms of burning pain. J E Biggs, J M Yates, A R Loescher, N M Clayton, F M Boissonade, P P Robinson. Brain Research, 1127; 59-65, 2007.