**2. Definition and pathophysiology of the trigeminocardiac reflex**

Since its first description in 1999, the TCR is defined as the sudden onset of parasympathetic dysrhythmia, sympathetic hypotension, apnoea or gastric hyper-motility during stimulation of any of the sensory branches of the trigeminal nerve [1]. The proposed underlying mechanism for the development of the TCR is that the sensory nerve endings of the trigeminal nerve send neuronal signals via the Gasserian ganglion to the sensory nucleus of the trigeminal nerve, forming the afferent pathway of the reflex arc [1, 2]. This afferent pathway continues along the short internuncial nerve fibres in the reticular formation of the pons to connect with the efferent pathway in the motor nucleus of the vagus nerve in the nucleus ambiguus (see Figure 1) [1]. Since this initial description, nearly all trigeminal innervated structures except Meckel's cave have been reported to lead to a TCR. Several lines of experimental evidence demonstrate that trigeminal induced cardiovascular reflexes could be excitatory evoked initially in the trigemi‐ nal nucleus caudalis and subsequently in the parabrachial nucleus, the rostral ventrolateral medulla oblongata, the dorsal medullary reticular field and the paratrigeminal nucleus [3, 17, 18]. Even so several studies on cellular level were performed, the exact cellular mechanism remains still to be explored.

**1. Introduction**

96 Abnormal Heart Rhythms

The fifth cranial nerve is the largest of all the cranial nerves and provides sensory supply to the face, scalp, sinus and mucosa of the nose and mouth as well as the dura mater of the middle, anterior and part of the posterior cranial fossa [1–3]. Stimulation of any of these sensory parts of trigeminal nerve has been shown to initiate the trigeminocardiac reflex (TCR) and also produce various cardiac arrhythmias besides other less life-threatening symptoms [1, 3, 4, 5]. Initially, this reflex has been studied in animals and is therefore known for more than a century [6–8], under the term of "trigemino-respiratory reflex" and now its revival as sudden infant death syndrome (SIDS). In the early 20th century, the TCR has gained much clinical and less experimental attention in the form of the oculocardiac reflex (OCR) which is the predominant cardiac response associated with the stimulation of the ophthalmic division of the trigeminal nerve during ocular surgeries [9, 10]. Then later, Schaller et al., for the first time, demonstrated that the TCR occurred with the stimulation of the intracranial portion of the trigeminal nerve as well [1]. In addition, Schaller and his group later sub-summarized all these reflexes under the term TCR [2, 11], what is now generally accepted. Since then, there have been extensive discussions about the reflex itself, about the prophylaxis or risk factors, about treatment and about the influence of the TCR on functional outcome when it occurs during the intracranial or the extra-cranial procedures. Schaller and his group could demonstrate the ubiquitary

occurrence of this reflex in any skull base procedure during 20 last years.

**2. Definition and pathophysiology of the trigeminocardiac reflex**

Since its first description in 1999, the TCR is defined as the sudden onset of parasympathetic dysrhythmia, sympathetic hypotension, apnoea or gastric hyper-motility during stimulation of any of the sensory branches of the trigeminal nerve [1]. The proposed underlying mechanism for the development of the TCR is that the sensory nerve endings of the trigeminal nerve send neuronal signals via the Gasserian ganglion to the sensory nucleus of the trigeminal nerve, forming the afferent pathway of the reflex arc [1, 2]. This afferent pathway continues along the short internuncial nerve fibres in the reticular formation of the pons to connect with the efferent pathway in the motor nucleus of the vagus nerve in the nucleus ambiguus (see Figure 1) [1]. Since this initial description, nearly all trigeminal innervated structures except Meckel's cave have been reported to lead to a TCR. Several lines of experimental evidence demonstrate that trigeminal induced cardiovascular reflexes could be excitatory evoked initially in the trigemi‐

rhythm changes related to the TCR.

The TCR also serves as an important interaction between brain and heart, and thus provides deeper understanding of mechanisms related to various cardiac changes related to various extra/intracranial surgeries [4, 12–16]. The TCR represents as a model for different other diseases like, for example, sudden infant death syndrome (SIDS). Therefore, this chapter highlights the various aspects of TCR including its definition, epidemiology, risk factors and management. Special consideration is given to illustrate the mechanism of various cardiac

**Figure 1.** Trigeminal nerve with trigeminal ganglion and nuclei (from Warwick, R, Williams PL. Gray`s Anatomy, 35th ed., p 1001, Edinburgh, Churchill Livingstone, 1973)

According to the current knowledge, the TCR occurs during the peripheral and central manipulations of the trigeminal nerve as well as around Ganglion Gasseri manipulation. The OCR, which is an accepted peripheral sub-form of the TCR, has been reported in patients with ocular surgeries and consecutive trigeminal nerve manipulations since several decades [9, 10, 19]. After 1999, as Schaller et al., for the first time, reported the occurrence of the TCR in skull base and neurological surgeries, it was thought that OCR and TCR are both the same reflex [1]. The underlying cellular mechanism is not yet fully understood (see Figure 2), but is believed to be the same as the TCR reported earlier on in more detail during activation of the central or intracranial portions of the trigeminal nerve [2].
