Trigeminocardiac reflex and SIDS

Gyaninder Pal Singh, Tumul Chowdhury, Barkha Bindu, Bernhard Schaller.  Sudden Infant Death Syndrome – Role of Trigeminocardiac Reflex: A Review.  Front. Neurol., 05 December 2016 https://doi.org/10.3389/fneur.2016.00221.  http://journal.frontiersin.org/article/10.3389/fneur.2016.00221/full?utm_source=newsletter&utm_medium=email&utm_campaign=Neurology-w1-2017

Sudden infant death syndrome (SIDS) is an unexplained death in infants, which usually occurs during sleep. The cause of SIDS remains unknown and multifactorial. In this regard, the diving reflex (DR), a peripheral subtype of trigeminocardiac reflex (TCR), is also hypothesized as one of the possible mechanisms for this condition. The TCR is a well-established neurogenic reflex that manifests as bradycardia, hypotension, apnea, and gastric hypermotility. The TCR shares many similarities with the DR, which is a significant physiological adaptation to withstand hypoxia during apnea in many animal species including humans in clinical manifestation and mechanism of action. The DR is characterized by breath holding (apnea), bradycardia, and vasoconstriction, leading to increase in blood pressure. Several studies have described congenital anomalies of autonomic nervous system in the pathogenesis of SIDS such as hypoplasia, delayed neuronal maturation, or decreased neuronal density of arcuate nucleus, hypoplasia, and neuronal immaturity of the hypoglossal nucleus. The abnormalities of autonomic nervous system in SIDS may explain the role of TCR in this syndrome involving sympathetic and parasympathetic nervous system. We reviewed the available literature to identify the role of TCR in the etiopathogenesis of SIDS and the pathways and cellular mechanism involved in it. This synthesis will help to update our knowledge and improve our understanding about this mysterious, yet common condition and will open the door for further research in this field…

Sudden infant death syndrome is the leading cause of death in the postneonatal period. The exaggeration of parasympathetic activity and cardiorespiratory response to hypoxia has been suggested as the possible mechanism for these events. Similarly, trigeminal air-stream stimulation (TAS) model also showed that the TAS may induce apnea and bradycardia in premature infants. In infants monitored for apparent life-threatening events, severe bradycardia was the most prevalent and predictive event seen in infants who succumbed to SIDS, and hypoxia is a frequent event that precedes death in infants of SIDS.

Interestingly, the laryngeal chemo-reflex (LCR), a protective mechanism, causes closure of the glottis, coughing, and apnea during aspiration of the fluid into larynx/trachea and, therefore, has also postulated as one of the causes of SIDS. On the other hand, DR, a subtype of TCR, has also been implicated to have a role in SIDS. The TCR is regulated by many brainstem nuclei and endogenously modulated by many neurotransmitters, the important one being serotonergic (5-HT), cholinergic (ACh), and nicotinergic. Abnormalities in the modulation of these neurotransmitters along with defect in brainstem nuclei maturation may lead to exaggerated TCR response…

Serotonergic or/and cholinergic dysfunction in the brainstem autonomic nuclei causes an exaggerated TCR response and thus culminates in sudden intense bradycardia, apnea, and death and, therefore, can be linked with the etiopathogenesis of SIDS. However, whether the exaggerated TCR response is the cause in all cases of SIDS is a subject for future research.