Abstract

Dear Sir, We have read with great interest the recent article of Prabhakar et al. [2] that points out some important aspects about how to prevent the trigeminocardiac reflex (TCR), which we have also pinpointed in our recent articles [5, 7, 9]. But the case report of Prabhakar et al. [2] is of great importance because it demonstrates clearly that application of intravenous anticholinergics to block the muscarinic receptors of the heart—either prophylactically or after the elicit of the reflex—cannot be alone a sufficient strategy to prevent further episodes of TCR [3, 4, 8] as it prevent the occurrence of bradycardia; this recommendation is especially and additionally based on (patho)physiological knowledge [3, 4]. One has therefore to assume that the (potential) adverse effects of epinephrine in combination with pretreatment by calcium-channel blockers eliminated by atropine in Prabhakar et al. case report [2] are evoked by a reflex response through the efferent vagus nerve. From our recent investigations, it seems that insufficient microsurgical technique with coagulation may be one of the principal risk factors of subsequent intraoperative occurrence of TCR. It seems that heat—for example by the use of bipolar coagulation—may impose a big risk for the trigger of the TCR [10]. However, it is interesting that Prabhakar et al [2] found that calcium-channel blocker could have been responsible for the occurrence of the TCR in their patient, an observation that we have made also in our initial report [8]. In this context, an interesting case series of Fujita et al. [1] demonstrates that topical anesthesia with lidocaine on the exposed trigeminal nerve may prevent circulatory turbulence based on a sodium channel blockade during skull base surgery, thus, avoiding an excessive increase of general anesthesia. We are far away to understand the TCR [6], but in the last months we have step by step gain further insights in this interesting and important phenomenon of skull base surgery [5]; not at least by the work of Prabhakar et al [2]. These findings may be in line with the suggestion that the TCR is a physiological, but not a pathophysiological entity [3]. Prevention will only be possible, if we better understand the physiology of this reflex.

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