New Molecular Knowledge Towards the Trigemino-Cardiac Reflex as a Cerebral Oxygen-Conserving Reflex

Abstract

The trigemino-cardiac reflex (TCR) represents the most powerful of the autonomous reflexes and is a subphenomenon in the group of the so-called “oxygen-conserving reflexes”. Within seconds after the initiation of such a reflex, there is a powerful and differentiated activation of the sympathetic system with subsequent elevation in regional cerebral blood flow (CBF), with no changes in the cerebral metabolic rate of oxygen (CMRO2) or in the cerebral metabolic rate of glucose (CMRglc). Such an increase in regional CBF without a change of CMRO2 or CMRglc provides the brain with oxygen rapidly and efficiently. Features of the reflex have been discovered during skull base surgery, mediating reflex protection projects via currently undefined pathways from the rostral ventrolateral medulla oblongata to the upper brainstem and/or thalamus, which finally engage a small population of neurons in the cortex. This cortical center appears to be dedicated to transduce a neuronal signal reflexively into cerebral vasodilatation and synchronization of electrocortical activity; a fact that seems to be unique among autonomous reflexes. Sympathetic excitation is mediated by cortical-spinal projection to spinal preganglionic sympathetic neurons, whereas bradycardia is mediated via projections to cardiovagal motor medullary neurons. The integrated reflex response serves to redistribute blood from viscera to the brain in response to a challenge to cerebral metabolism, but seems also to initiate a preconditioning mechanism. Previous studies showed a great variability in the human TCR response, in special to external stimuli and individual factors. The TCR gives, therefore, not only new insights into novel therapeutic options for a range of disorders characterized by neuronal death, but also into the cortical and molecular organization of the brain.

Sudden Infant Death Syndrome – Role of Trigeminocardiac Reflex: A Review

“…This is due to intense peripheral vasoconstriction caused by more strong sympathetic stimulation during DR than during peripheral TCR (42). This reflex also persists in humans and is probably inherited from diving birds and amphibians (18, 32, 43–45). It is particularly prominent in infants and manifests as severe bradycardia upon a single submersion of the face in the water (46, 47).…”

The Trigeminocardiac Reflex in Neurological Disorders

“…Its occurrence can lead to varied clinical presentations ranging from bradycardia and hypotension to complete asystole and/or apnea. [1][2][3][4][5][6][7][8] Because of these potentially life-threatening complications, the TCR has gained enormous and increasing attention during the last several years.…”

“…1 It is generally accepted that the diving reflex and ischemic tolerance appear to involve at least somewhat similar physiological mechanisms. [5][6][7][8] The presence of such endogenous neuroprotective mechanisms may expand the spectrum of the TCR beyond its actually known clinical appearance, to include the prevention of other potentially brain injury states as well.…”

“…[5][6][7] The reflex has been shown to cause cerebral vasodilatation and increase the cerebral blood flow without increasing the cerebral metabolic rates of oxygen and glucose. [5][6][7] Cerebral vasodilatation may be a secondary response aimed at overcoming hypoxemia due to hypotension and apnea induced by the TCR. The concomitant increase in carbon dioxide, caused by bradypnea or apnea, may be responsible for causing this protective cerebral vasodilatation, as has been described in the case of oxygen-conserving reflexes.…”

“…[1][2][3][4][5][6][7][8] The proposed reflex arc involves the stimulation of sensory nerve endings-the sensory branches of the trigeminal nerve that carry neuronal signals to the sensory nucleus of the trigeminal nerve via the Gasserian ganglion, which forms the afferent pathway of the reflex arc. [1][2][3][4][5][6][7][8] The internuncial nerve fibers in the reticular formation connect the sensory nucleus…”