Vagoglossopharyngeal-associated syncope due to a retained bullet in the jugular foramen

Abstract

Gunshot wounds (GSWs) to the head are frequently fatal. Rarely, the bullet may lodge in the skull base and not cause significant brain injury. Typically, the bullet fragments are felt to be inert and do not require operative extirpation if they are within the bony confines of the skull base. We report the case of a bullet in the jugular foramen causing recurrent syncope that resolved after surgical removal of the bullet. The medical records from a patient who suffered a GSW to the head were retrospectively reviewed and the treatment and outcome documented. In 2000, a 20-year-old man suffered a GSW to the head. Immediate evaluation revealed the bullet in the right skull base at the jugular foramen, but no parenchymal brain injury. One year after the GSW, he began to experience stereotypical spells resulting in loss of consciousness. Extensive cardiovascular workup was normal. In 2002, the patient underwent removal of the bullet. He has been syncope-free since the operation and returned to his career in the military. We believe the retained bullet in this patient was irritating the IX-X cranial nerves, resulting in syncope, similar to the mechanism in vagoglossopharyngeal neuralgia. Removing the bullet relieved the irritation and stopped the syncopal spells.

Keywords: Gunshot wounds; Syncope; jugular foramen; vagoglossopharyngeal neuralgia.

Figure 1

Lateral radiograph reveals a large-caliber bullet in the region of the right skull base/inferior jugular foramen.

Figure 2

Axial computed tomographic scans confirm the bullet is located in the inferior right jugular foramen.

Figure 3

Right common carotid artery injection demonstrates occlusion of the right internal carotid artery known to be secondary to gunshot wound.

Figure 4

The intact bullet after removal.

Figure 5

Red: General visceral afferents from IX and X. Blue: Preganglionic parasympathetic efferents. Green: The solitary nucleus sends excitatory input to the dorsal vagal nucleus that increases parasympathetic outflow to the heart, resulting in bradycardia. It also sends inhibitory input to the rostral ventrolateral medulla, reducing firing in the intermediolateral cell column of the spinal cord, reducing sympathetic outflow to the blood vessels and causing associated vasodilatation.