A 54-year-old man with history of tobacco use presented to the Emergency Department with a few-hour history of dizziness and 2-month history of intermittent right jaw pain. His blood pressure was 68/48 mm Hg, heart rate was 55 beats per minute, and oxygen saturation was 85% on room air. Physical examination was notable for a swelling on the right side of the hard palate and a right abducens nerve palsy. Laboratory testing was unremarkable. Electrocardiogram showed sinus bradycardia. A facial computed tomography scan with contrast was obtained and showed a 3-cm solidly enhancing mass in the right maxilla causing destruction of the surrounding bony structures, suggestive of aggressive malignancy and less likely an infectious process. Given the hypotension and hypoxia, sepsis was considered the more likely diagnosis initially. A subsequent magnetic resonance imaging scan demonstrated a 2.8 × 2.0 × 3.0-cm enhancing mass centered in the right maxilla with extension along the right trigeminal nerve up to the surface of the midbrain. Biopsy of the mass revealed adenocarcinoma. He then underwent right palatectomy with maxillectomy with reconstruction followed by radiotherapy. His bradycardia resolved after completion of radiotherapy, thus confirming the presence of the trigeminocardiac reflex.
The trigeminocardiac reflex is defined as the acute onset of cardiac dysregulation manifesting as hypotension and bradycardia, hypopnea, and gastric hypermotility, which are brought on by mechanical stimulation of the trigeminal nerve or any of its branches. To diagnose a patient with trigeminocardiac reflex, 2 of the following must be present: 1) symptoms explainable by an adequate stimulation of the trigeminal nerve, 2) the symptoms appear promptly after the applied stimulus, and 3) the symptoms disappear and cardiopulmonary functions return to baseline shortly after stimulus removal.1
The mechanism of the trigeminocardiac reflex starts with stimulation of any portion of the trigeminal nerve or the trigeminal ganglion (Figure). This stimulus sends afferent neuronal signals to the trigeminal nerve sensory nucleus in the medulla, where short internuncial neurons of the reticular formation connect with efferent parasympathetic neurons in the motor nucleus of the vagus nerve. Stimulation of the vagus nerve is responsible for the cardiac bradyarrhythmia, hypotension, and gastric hypermotility.2 Although the mechanism of the hypopnea and apnea is not completely understood, it might be due to stimulus alterations in neurons responsible for respiratory rhythm generation in the ventrolateral medulla, which lies adjacent to both the trigeminal nerve nucleus and the efferent parasympathetic neurons of the vagus nerve.2
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-Jason M. Lunt, DO, Ahmad Al-Taee, MD, Rachna Rawal, MD, Fred R. Buckhold III, MD
This article originally appeared in the November 2017 issue of The American Journal of Medicine.
