Physical Address
304 North Cardinal St.
Dorchester Center, MA 02124
Trigeminocardiac Reflex
Definition
The trigeminocardiac reflex (TCR) is a reproducible brain stem reflex originating as a result of stimulation of the trigeminal nerve (anywhere along its course) and manifests as a sudden development of cardiac dysrhythmia up to asystole, arterial hypotension, apnea, and gastric hypomotility. However, under general anesthesia, the classically described symptoms may not be appreciated, other than cardiac dysrhythmia and arterial hypotension. It is then defined by reduction in the mean arterial pressure and the heart rate by more than 20% of its baseline values coinciding with the stimulation of the trigeminal nerve.
First described as the Kratschmer’s reflex in cats and rabbits, this reflex is now being increasingly studied. This intraoperative phenomenon not only occurs during neurosurgical procedures but also during maxillofacial, ophthalmic, nasal, dental, and skull-base surgeries. Interestingly, the reflex can be elicited by stimulation of any of the three divisions of the fifth cranial nerve, that is, ophthalmic, maxillary, or mandibular nerves.
Pathophysiology
The physiological mechanism of the TCR is that following stimulation of the sensory nerve endings of the trigeminal nerve, signals are sent to the sensory nucleus of the trigeminal nerve via the Gasserion ganglion. This afferent pathway continues along the short internuncial nerve fibers in the reticular formation to connect with the efferent pathway in the motor nucleus of the vagus nerve. Depressor fibers of the vagus nerve end in the myocardium, leading to autonomic changes ( Figure 1 ).
The Flowchart Below Explains the Pathway
Sensory nerve endings of trigeminal nerve → Gasserian ganglion → Trigeminal nerve → Superficial medullary dorsal horn and sensory nucleus of trigeminal nerve → via short internuncial neurons to vagal motor nucleus → vagus nerve → depressor fibers from vagus ending in myocardium.
It is suggested that the parasympathetically mediated bradycardia, sympathetically-mediated vasoconstriction, and the central inhibition of the respiratory rhythm (apnea) must be modulated by the trigeminal system within the brainstem. It must be remembered that the autonomic nervous system activation is central to the occurrence of TCR. It is suggested that the coactivation of the sympathetic and parasympathetic systems may be involved in the occurrence of the TCR. It is known that the autonomic influences on heart are generally weak. Parasympathetic fibers primarily innervate the atria and the conducting tissues, whereas sympathetic fibers are more widely distributed throughout the heart. Therefore, vagal effects frequently have a rapid onset and resolution; whereas, sympathetic influences generally have a gradual onset and dissipation. It has been suggested that myelination status of the nerve may not be an important risk factor and phenotypic heterogeneity could be the basis of susceptibility for simultaneous autonomic nerve activation.
You're Reading a Preview
Become a Clinical Tree membership for Full access and enjoy Unlimited articles
If you are a member. Log in here