Stimulation of cranial nerves modulates central nervous system (CNS) activity via the extensive connections of their brainstem nuclei to higher-order structures. Clinical experience with vagus-nerve stimulation (VNS) demonstrates that it produces robust therapeutic effects, however, posing concerns related to its invasiveness and side-effects. Trigeminal nerve stimulation (TNS) has been recently proposed as a valid alternative to VNS. The ear presents afferent vagus and trigeminal-nerve distribution; its innervation is the theoretical basis of different reflex therapies, including auriculotherapy. An increasing number of studies have shown that several therapeutic effects induced by invasive VNS and TNS, can be reproduced by noninvasive auricular-nerve stimulation. However, the sites and neurobiologic mechanisms by which VNS and TNS produce their therapeutic effects are not clear yet. Accumulating evidence suggests that VNS and TNS share multiple levels and mechanisms of action in the CNS.

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In the present study the possible derangement of the autonomic system and its influence in life threatening arrhythmias were analysed during paroxysmal activity. In hemispherectomized rats a paroxysmal activation of the hypothalamic and mesencephalic cardioarrhythmogenic triggers was performed by topical application of penicillin-G. Blood gas parameters and electrical activity of the thalamus, hypothalamus, vagal nerve fibre, ECG and arterial blood pressure were simultaneously monitored in basal conditions and repeated after the appearance of paroxysmal activity. Temporal correlation analysis was carried out. Results showed that during activation of these triggers, the spontaneous vagal nerve fibre activity significantly increased and triggered the appearance of cardiac arrhythmias which could become life threatening and induce animal death when blood gas and electrolytic parameters were simultaneously impaired. These experiments suggest that fatal evolution of the heart impairment is related not only to an autonomic cardiac trigger, but also to a concomitant metabolic derangement, which most likely shares the same autonomic origin.

Sound is a natural stimulus for both cochlear and saccular receptors. At high intensities it evokes in active masseter muscles of healthy subjects two overlapping reflexes: p11/n15 and p16/n21 waves, whose origin has not yet been demonstrated. Our purpose was to test which receptor in the inner ear is responsible for these reflexes. We compared masseter EMG responses induced in normal subjects (n = 9) by loud clicks (70-100 dB normal hearing level (NHL), 0.1 ms, 3 Hz) to those evoked in subjects with a selective lesion of the cochlea (n = 5), of the vestibule (n = 1) or with mixed cochlear-vestibular failure (n = 5). In controls, 100 dB clicks induced bilaterally, in the unrectified mean EMG (unrEMG), a clear p11 wave followed by a less clear n15 wave and a subsequent n21 wave. Lowering the intensity to 70 dB clicks abolished the p11/n15 wave, while a p16 wave appeared. Rectified mean EMG (rectEMG) showed, at all intensities, an inhibitory deflection corresponding to the p16/n21 wave in the unrEMG. Compared to controls, all deaf subjects had a normal p11 wave, together with more prominent n15 wave; however, the p16/n21 waves, and their corresponding inhibition in the rectEMG, were absent. The vestibular patient had bilaterally clear p11 waves only when 100 dB clicks were delivered bilaterally or to the unaffected ear. Stimulation of the affected ear induced only p16/n21 waves. Data from mixed patients were consistent with those of deaf and vestibular patients. We conclude that click-induced masseter p11/n15 waves are vestibular dependent, while p16/n21 waves depend on cochlear integrity.