Persistent Premature Atrial Contraction as the Sole Presentation of Trigeminocardiac Reflex during Radiofrequency Thermocoagulation
The trigeminocardiac reflex (TCR) consists of sudden-onset bradycardia, hypotension or hypertension, apnea, or gastric hypermotility due to the stimulation of any of the sensory branches of the trigeminal nerve.1 The occurrence of TCR has been reported during craniofacial surgery, tumor resection in the cerebellopontine angle, and percutaneous balloon microcompression or glycerol rhizolysis2 of the trigeminal ganglion. A 75-year-old man weighing 70 kg, with trigeminal neuralgia in the distribution of the left mandibular division (V3), was posted for radiofrequency thermocoagulation (RFT) under fluoroscopic guidance. His medical history was unremarkable and the baseline electrocardiogram (ECG) was normal. In the operation theater, intravenous access was secured and routine monitors such as ECG, noninvasive blood pressure, and SpO2 were connected. Dexmedetomidine 10 μg/kg (bolus) followed by 0.5 μg/kg/h (maintenance) was administered for procedural sedation. Oxygen was supplemented through a nasal cannula at 2 L/min with simultaneous end-tidal carbon dioxide monitoring. Under all aseptic precaution, the Hertel technique was followed to place a standard 10-mm 20-G needle with a stylet into the trigeminal cistern. When the needle tip entered into the foramen of the ovale, premature atrial contractions (PACs) appeared on the ECG (Fig. 1A), which was synchronous with the dysrhythmia seen in the pulse oximetry waves. The needle tip was then placed adjacent to the V3 division in the trigeminal cistern. The dysrhythmia persisted without any further hemodynamic perturbations. Hence, we decided to continue with the procedure. Stimulation of the nerve was carried out to confirm the affected division (V3), and lesioning was performed uneventfully. Three cycles of RFT were performed at a temperature ranging from 70 to 90°C, for 60 seconds each. At the completion of the procedure, the needle was withdrawn, which was followed by spontaneous resolution of the PACs (Fig. 1B). The patient had complete relief of neuralgic pain on the affected side.
TCR is a relatively known complication during percutaneous ablative procedures involving the trigeminal nerve, and dysrhythmia such as bradycardia and asystole have been observed with its occurrence. However, PAC as a sole presentation of TCR during the RFT has never been mentioned. Trigeminal sensory nerve fibers send signals through the gasserian ganglion to the sensory nucleus, forming the afferent pathway of the TCR. This afferent pathway continues through the internuncial nerve fibers in the reticular formation to connect with the efferent pathway in the motor nucleus of the vagus nerve.3 Stimulation of the trigeminal nerve anywhere along its peripheral course (after the gasserian ganglion) results in TCR, which would coactivate the parasympathetic and the sympathetic systems.4 Hence, the patient presents with bradycardia and hypertension. Instead, in our patient, persistent PACs possibly occurred owing to excessive sympathetic stimulation apart from the parasympathetic stimulation, thereby producing the abnormal the cardiac responses. The use of dexmedetomidine probably controlled the blood pressure to a normal range instead of resultant hypertension with sympathetic stimulation. The patient had a stable hemodynamic course despite persistent dysrhythmia, and therefore, we did not abandon the procedure and were confident in proceeding with a good outcome.