Sir, we would like to report the case of a 58-year-old female who was referred to a maxillofacial unit by her dentist, with persistent numbness and altered hearing, following a buccal infiltration (1 ml 2% lignocaine with 1:80,000 adrenaline) for periodontal treatment in the upper right seven region. She had a medical history of myocardial infarction, unstable angina, hypertension, asthma, hypercholesterolaemia, diet controlled diabetes mellitus and osteoarthritis and was taking several medications, none of which interact with local anaesthetic.

Clinical examination revealed diminished sharp and blunt discrimination of the first and second divisions of the right trigeminal nerve. No other abnormality was found. Intraorally there was tenderness of the buccal gingivae adjacent to the upper right second molar tooth, which was also tender to percussion but vital. An ENT opinion was sought in relation to the auditory acuity, but no abnormalities were diagnosed and no further investigations were required. Diagnoses of right first and second division trigeminal neuropathy, reduced auditory acuity and tinnitus were made. At two week review the upper right seven was extracted. After ten months there was limited recovery of the trigeminal nerve, but the reduced auditory acuity and tinnitus were still present. An audiogram and MR imaging arranged at this stage were reported as normal. Interestingly, at this review bilateral temporomandibular joint dysfunction was found.

The exact mechanism causing these symptoms is unknown; the following theories have been proposed:

  • Retrograde anaesthetic vasoconstrictor access to the middle ear via venous system resulting in vasospasm of the cochlear division of the internal auditory artery, leading to vestibulocochlear nerve dysfunction1

  • Nerve damage following direct needle penetration2 or upon withdrawal of a barbed needle.2,3 Such barbs rupture the perineurium, herniate the endoneurium and cause transection of nerve fibres2

  • Tinnitus due to temporomandibular joint dysfunction4

  • Neuropraxia from intraneural haematoma due to intraneural blood vessel trauma, leading to constrictive epineuritis.2 An initial phase of neurotoxicity is followed by reactive fibrosis which inhibits nerve healing2

  • Neurotoxicity produced by LA solution deposited intraneuerally.2 Chemical trauma also causes demyelination, axonal degeneration, oedema and inflammation, of the nerve fibres.2 The endoneurial oedema causes ischaemia, followed by a period of reperfusion, during which reactive free radicals produce cytotoxic nerve injury.2 If the LA solution is highly concentrated there is an increased chance of neurotoxicity.2

Spontaneous complete recovery from the altered sensation occurs within eight weeks in up to 95% of cases.2 However, patients with paraesthesia of longer duration after injury, have less chance of a full recovery despite attempts at microneurosurgical decompression.2

This case highlights that unusual events can occur following a common procedure in dental practice.