The Relationship of the Trigemino-Cardiac Reflex to Sleep Bruxism

Abstract

nerve at any course along its distribution. Stimulation of the TCR results in neuronal signals being transmitted via the trigeminal nerve to the GGa; continuing to the sensory nucleus of the trigeminal nerve (V5) in the brain stem (mesencephalic nucleus). Signals are then transmitted polysynaptically through the reticular formation (RF); via short internucial fibers; to the dorsal motor nucleus of the vagus nerve (X). This pathway is considered as an afferent to the TCR (Figures 1-3). Parasympathetic neurons comprise much of reflex; arising in the motor nucleus of V5. Stimulation of V5 results in bradycardia; hypotension; as well as apnea and gastric hypermobility [17]. The reflex is of utmost importance during surgical procedures adjacent to the branches of the trigeminal nerve as the TCR can inadvertently be stimulated compromising the surgical procedure [18-21]. In procedures near or in the GGa; the opposite effect may be encountered: tachycardia; tachypnea and hypertension and gastric hypomobility [22,23]. Figure 1: The Trigemino-Cardiac Reflex. Stimulation of the trigeminal nerve from branches V2 and V3 result in stimulation of the TCR very differently from V1, peripheral nerves and post-Gasserion ganglion regions. V2 and V3 can stimulate an increase in heart rate, respiration and blood pressure as opposed to a decrease as seen in the other regions. Only free nerve endings in the periodontal ligaments, the mental nerve and afferents from spindles in the masseter and temporalis muscles act to initiate the stimulation of the TCR at the level of the gasserion ganglion. External sensory nerves of V2 and V3 act to stimulate the TCR as expected. Short internucial fibers in the reticulum formation connect the trigeminal sensory nucleus down to terminate at the dorsal motor nucleus and vagus nerve. V1 V2 V3 Figure 2: Sleep tracing demonstrating the TCR and Sleep Bruxism. This sleep study tracing demonstrate the effect of sleep bruxism on the TCR. The heart rate increases to 100bpm from 74bpm (a 26% increase) in response to the major SB event. There is also an increase in respiratory effort seen (blue dashed square). The effect disappears immediately after the SB stops. The stimulation of the TCR is obviously occurring at the level of the Gasserion ganglion. In this example, no respiratory events (central or obstructive apneas, hypopneas) occurred and the blood oxygen levels (Sp02) remained constant throughout (98-99%). The minor SB events (blue arrow) do not stimulate the TCR, only the major events do. This tracing demonstrates plausibility and reversibility of the TCR. It also demonstrates a lighter stimulation does not activate the TCR. This meets 4 of the cause and effect criterion proposed by Meuwly et al. (Table 2).