**4. Heart and the trigeminocardiac reflex**

The TCR is a clinical phenomenon that reflects interactions of many organs to the brain [4, 12, 14, 19, 29–31]. Among all the organs, the connection between heart and brain is unique and presents a wide array of clinical manifestations when the TCR gets incited [16]. These clinical signs include drop in heart rate and blood pressure, asytole, ventricular tachycardia/fibrilla‐ tion, ST-T wave changes and other forms of arrhythmias [4, 5, 12–16, 29, 31–65]. Stimulus especially in form of stretch has found to be the strongest inciting factor for the TCR [1]. However, mild stimulus may also results into TCR episodes [3, 18, 35]. Chowdhury et al. reported that mild stimulus in the form of skin closure could able to produce transient asystole and questioned about the severity of stimulus and TCR manifestation. In another report, Chowdhury et al. further suggested that various manifestations of TCR episodes (bradycardia, hypertension, asystole) as well as different subtypes of TCR (peripheral and central) could manifest in the same patient [4, 13]. Again, in this report, transient asystole manifested during the skin closure as well [4]. Author postulated that the different sympathetic outflow responses could be due to different depths of anaesthesia, which coupled with different forms of TCR stimulation probably contributed to different haemodynamic responses in the same patient and obscured the classical manifestation of TCR [3]. Strikingly, the cardiovascular changes of TCR phenomenon mainly reported due to acute stimulation (peri-operatively) of trigeminal nerve; however, Chowdhury and Schaller highlighted the first description of chronic form of TCR [40].

As highlighted in a review by Chowdhury et al., the other rare cardiac perturbation i.e. coronary spasm in neurosurgical patients may be the mere manifestation of TCR events [16]. In this case series review, author found that in most of the neurosurgical conditions, dural stimulation provoked the ST-T wave changes, ventricular tachycardia and ventricular fibrillation [16]. The vagal mediated acetylcholine receptors have been also linked with the development of spasm [16]. Though majority of coronary spasm events were of transient nature (few minutes to few hours); however, very few of them also developed perioperative myocardial infarction.
