Parasympathetic activity originates in vari­ous areas within the brainstem. The fibers that control the pupil sphincter muscles originate in the Edinger-­Westphal nuclei of the CN III nuclear complex within the midbrain. The main input to the Edinger-­Westphal nuclei is from the pretectal nuclei, both directly and via the posterior commissure. In turn, the pretectal nuclei receive input directly from the afferent visual pathways via the pupillary tract, which leaves the optic tract in the brachium of the SC just anterior to the LGN (Fig 1-47). Lesions of the brachium of the SC can cause a contralateral RAPD, whereas lesions of the LGN do not cause this defect. The cortex (especially the frontal lobes), the hypothalamus, and the reticular activating system provide tonic inhibitory signals to the Edinger-­Westphal nuclei. During sleep, loss of this inhibitory activity ­causes the pupil to become smaller. In addition, the Edinger-­Westphal nucleus receives input from the more ventral and rostral midbrain, prob­ably related to bitemporal image disparity that serves as a stimulus for convergence and the near reflex.

The parasympathetic fibers and the CN III fascicles leave the CN III nucleus and exit the brainstem ventrally in the interpeduncular fossa. Within the subarachnoid space, the para­ sympathetic fibers tend to run on the medial superficial surface of CN III. When CN III bifurcates in the anterior cavernous sinus, the parasympathetic fibers travel with the inferior division. In the orbital apex, ­these fibers synapse in the ciliary ganglion (unlike the sympa­ thetic and nasociliary fibers, which travel through the ganglion without synapse). The post­ synaptic fibers then travel with the branch destined for the inferior oblique muscle, joining the short posterior ciliary nerves to reach the anterior segment and the iris sphincter muscles. The sphincter muscles collectively are approximately 0.8 mm in dia­meter and 0.15 mm thick. They travel circumferentially around the pupillary margin just anterior to the posterior pig­ mented epithelium and central to the termination of the dilator muscle cells. The muscles are made up of units of 5–8 muscle cells each.

Parasympathetic innervation to the lacrimal gland originates in the superior saliva­ tory (salivary) nucleus located in the caudal pons posterolateral to the motor nucleus of CN VII (see Fig 1-45). This nucleus receives sensory input from CN V and additional afferent fibers from the hypothalamus. Efferent parasympathetic fibers for lacrimal, mu­ cous, and salivary secretion exit the nucleus, joining other parasympathetic efferent fibers coming from the salivatory nucleus and traveling with afferent gustatory fibers from the anterior two-­thirds of the tongue in the nervus intermedius. The gustatory fibers synapse in the nucleus of the tractus solitarius parallel to the fascicles of CN VII in the nervus intermedius (see Fig 1-44). This nerve joins CN VII to exit the brainstem on its ventral surface at the pontomedullary junction. Together with the other fascicles of CN VII, the parasympathetic fibers of the nervus intermedius run laterally to the internal auditory meatus. Within the petrous bone and fallopian canal, the parasympathetic fibers exit at the geniculate ganglion and then travel superficially over the petrous bone with the greater superficial petrosal nerve. This course parallels that of the ICA. In the area where the ICA turns to rise into the cavernous sinus, the fibers join the vidian nerve, which then travels through the sphenoid bone parallel to and beneath the foramen rotundum to enter the pterygomaxillary space. The fibers synapse in the sphenopalatine ganglion (see Fig 1-45). The postganglionic fibers travel superiorly through the inferior orbital fissure and then with the lacrimal nerve to innervate the lacrimal gland. This pathway is also responsible for reflex tearing.