Pathways for orofacial pain sensation in the trigeminal brain-stem nuclear complex of the Macaque monkey.

Eleven Macaque monkeys underwent a variety of lesions in the trigeminal afferent system; namely, tractotomy, rhizotomy, and radiofrequency destruction of various components of the bulbospinal trigeminal nuclear complex. Behavioral responses were evaluated before and after the lesions using a quantitative paradigm which measured lever-pressing in response to electrical stimulation of the dental pulp or facial skin, and by assessing adversive responses to facial cutaneous and intraoral pin-scratch. Thresholds for lever-pressing in response to cutaneous facial stimulation were elevated by tractotomy, elevated further by a combination of tractotomy and rhizotomy of the seventh, ninth, and 10th cranial nerves and cervical dorsal roots C1-3, and maximally elevated by complete radiofrequency destruction of the trigeminal nucleus caudalis. These lesions also abolished adversive responses to cutaneous facial pin-scratch. None of these lesion combinations, however, altered lever-pressing responses to dental pulp stimulation. Radiofrequency destruction of the trigeminal nuclei principalis, oralis, and interpolaris caused elevations of lever-pressing thresholds in response to dental pulp stimulation, and also smaller but statistically significant elevations on cutaneous electrical stimulation. Mild reductions in adversive responses to cutaneous pin-scratch were also produced by these rostral nuclear lesions, suggesting analgesia. The experiments suggest that primary afferent fibers for dental pain perception travel only in the trigeminal nerve and that these fibers relay via the trigeminal brain-stem nuclei principalis, oralis, and interpolaris. Primary afferent fibers for cutaneous facial pain perception travel in the trigeminal, facial, glossopharyngeal, and vagus nerves, and the upper cervical dorsal and ventral roots, and these afferents relay mainly in the trigeminal nucleus caudalis.