Local anesthesia is an indispensable aid in a dentist’s practice and, from a purely pharmacological point of view, it stands out positively for efficacy and safety.
In some cases, however, conventional anesthetic infiltration techniques result in difficulties linked to control of the syringe and to the diffusion of the solution within delicate spaces of the skull. This can lead to the occurrence of even significant complications, which can lead to various consequences, starting from the interruption of the planned dental procedure.
The abducens consists of the sixth pair of cranial nerves and, unlike the trigeminal nerve, whose terminal branches are the target of local dental anesthesia, it is made up of exclusively motor fibers. The nerve controls the movement of the lateral rectus muscle which, by contracting, rotates the eyeball outwards on the horizontal plane; a movement that in fact, similarly to what it is called for limbs, is defined as abduction.
Since the nerve conduction system is completely analogous, the somatic motor fibers can be the target of local anesthesia as much as the trigeminal sensitive ones.
The onset of paralysis consists of weakness or functional deficit at the muscle level and can occur on a pathological, idiopathic or, precisely, iatrogenic basis.
Paralysis of the abductor nerve, albeit rarely, can occur in iatrogenic form as a complication of local dental anesthesia maneuvers. In particular, the procedures at greatest risk are the Inferior alveolar nerve block (45.8%), and the posterior superior alveolar nerve block (40.3%).
Local anesthesia and complications to the abducens nerve
Clinically, paralysis occurs with the onset of diplopia and strabismus, determined by a blocked ipsilateral abduction, possibly associated with vertigo. Since it is a pharmacological and non-trauma based complication, it is characterized by constant transience, which normally follows the effective range of the local anesthetic. Rarely, cases require an ophthalmologist’s consultation. An intervention will however, mostly relieve symptoms. In most cases, it will be sufficient for the dentist to reassure the patient and monitor the latter during the postoperative period.
From an anatomical point of view, the path of the abducens nerve should actually be protected against this type of involvement. Some authors have proposed plausible theories about this.
One of these theories involves involuntary administration through the internal maxillary artery, which is followed by a spread across the vascularization area, up to the middle meningea and, via the anastomotic route, to the tear duct.
More likely is the theory that envisages intravenous diffusion, starting from the pterygoid plexus, up to the cavernous sinus; the nerve would be exposed to this complication precisely at the level of its intracavernous tract.
Considering the nerve path, the diffusion of the anesthetic solution through the pterygopalatine fossa and the lower orbital fissure, up to the apex of the orbital cavity, where the nerve runs, can also be hypothesized. Involvement from the major palatal canal is more difficult, given the distance of the nerve; this could become likely in the presence of anatomical variations.