Extracranial involvement of the recurrent laryngeal nerve and the hypoglossal nerve is known as Tapia syndrome
1-3). Our patient developed this combination of abnormalities immediately after decompressive laminectomy performed by the posterior approach. The combination injury of the hypoglossal and vagal nerves due to extracranial involvement is very rare. The vagal nerve leaves the cranium through the jugular foramen and passes through the neck to the thorax. The 9
th, 10
th and 11
th cranial nerves are anterior to the internal jugular vein (IJV) as they traverse the jugular foramen. They are immediately posterior to the internal carotid artery (ICA) as they emerge from it. The superior and inferior sensory ganglion of the 9
th and 10
th nerve are seen as thickening immediately inferior to their exit from the cranium(
Fig. 3A). The hypoglossal nerve is medial to the 9
th, 10
th and 11
th cranial nerves after they exit the cranium through the hypoglossal canal. The hypoglossal nerve descends to the anterior cervical region; along this path it is near to the surface of the inferior vagal ganglion (
Fig. 3B). Then the hypoglossal nerve crosses the vagal nerve in order to continue its route medially and ultimately reaches the tongue and supply all the extrinsic muscle of the tongue
5). This close relationship between the vagal and hypoglossal nerve explains why both nerves can be injured simultaneously
2,3,6,9). The main causes of Tapia syndrome are tumors or injury to the upper neck as well as congenital and idiopathic lesions including iatrogenic causes such as endotracheal intubation
7-9). There are recent reports in the literature on Tapia syndrome after oro-tracheal intubation resulted from compression by the cuff pressure of the endotracheal tube and prolonged stretching of cranial nerves by improper positioning of the head
9). Namely, poor and inadequate body position during surgery may cause the Tapia syndrome. Boisseau et al. reported the Tapia syndrome following shoulder surgery caused by fully upright sitting position
2). He presumed cranial nerve injuries could occur due to compression by the tracheal tube resulted from excessive displacement of the head. Moreover, the endotracheal tube might have caused symptoms in this patient such as disturbance of laryngeal function and swallowing. In our patient, transoral intubation was performed without any problem, the pressure was checked regularly, and nitrous oxide was not given. In fact, we do not know exact etiology of these cranial nerves paralysis. However, we speculate the involved possible mechanisms include compression of nerves against the mandible by excessive anterior flexion of neck or stretching of the cranial nerves by the tracheal tube itself or the cuff pressure in spite of regular pressure check
3). So, we believe that although neck flexion is necessary for posterior prone position, we would recommend avoidance of excessive prolonged hyperflexion of the neck and adequate cuff pressure during surgery. Although steroids are most commonly used to treat these cranial nerve palsies, there is no definitive therapy. In some cases, administration of steroids and vitamins may be used to shorten the recovery period
4,7). We followed our patient for eight months but the symptoms were not improved despite conventional steroid therapy.