Abstract Glossopharyngeal neuralgia-asystole syndrome (GN-AS) is a rare neurocardiogenic disorder in which paroxysms of sharp pain within the glossopharyngeal nerve territory trigger excessive vagal activation, resulting in bradycardia, hypotension, syncope, or even transient cardiac arrest. These events occur when afferent impulses from cranial nerve IX reflexively stimulate vagal efferent pathways in the medulla. Although GN-AS can occur idiopathically, it more often arises from secondary causes that irritate or compress the lower cranial nerves. Head-and-neck tumors, particularly tonsillar carcinoma, may provoke both neuralgic pain and cardioinhibitory syncope through local invasion of the glossopharyngeal and vagus nerves. A 55-year-old man with right-sided heart failure and recently diagnosed left tonsillar squamous cell carcinoma presented after his first radiation session with dizziness, nausea, and hypotension. While in the emergency department, his heart rate abruptly dropped to the 20s, followed by unresponsiveness and loss of pulse. A code blue was initiated; atropine and brief chest compressions restored circulation. ECG showed sinus rhythm with first-degree AV block and right bundle-branch block, unchanged from baseline. Laboratory results and troponin were unremarkable. During ICU monitoring, he experienced recurrent sharp left-sided jaw and throat pain followed within seconds by diaphoresis, bradycardia, and hypotension, each resolving after atropine. He subsequently had another brief cardiac arrest characterized by unresponsiveness and loss of pulses, with restoration of circulation following atropine administration. Neck CT demonstrated a soft-tissue mass at levels II-III consistent with known malignancy, and prior PET imaging had shown bulky level II-III cervical lymphadenopathy encasing the left carotid bifurcation and proximal internal carotid artery. The presentation was concerning for glossopharyngeal neuralgia-asystole syndrome. AV-nodal-blocking agents were discontinued, and carbamazepine plus corticosteroids were initiated for neuralgic pain and peritumoral edema. No further bradyarrhythmic episodes occurred thereafter. GN-AS is estimated to occur in 0.2-0.7 per 100,000 person-years. Reflex asystole results from intense vagal efferent discharge triggered by glossopharyngeal pain, often precipitated by swallowing, chewing, or talking. Differentiation from carotid-sinus hypersensitivity is essential, as the latter is painless and induced by neck movement or pressure. Recognition of the pain-preceding bradyarrhythmia pattern enables prompt neuralgic control and prevention of recurrent asystole. Glossopharyngeal neuralgia-asystole syndrome should be considered in patients with head-and-neck malignancy who develop pain-triggered bradycardia or syncope, as timely recognition and treatment can be lifesaving. This abstract is funded by: None
Alrashdan et al. (Fri,) studied this question.