The findings indicated a lesion of the postganglionic (third order) sympathetic neuron, either primary or by transsynaptic degeneration. Some axons of the postganglionic neuron must have been intact, because the synkinesis requires adrenergic innervation of the iris dilator muscle. There is a close topographic relationship among the sympathetic superior cervical ganglion, the inferior ganglion of the vagus nerve, the hypoglossal nerve, and the glossopharyngeal nerve.1 The esophagus and stomach atony and the recurrent laryngeal nerve paresis indicate an injury to vagal fibers. The swallowing disorder, the flacidity of the soft palate, and the remaining deviation of the extended tongue indicate involvement of hypoglossal and glossopharyngeal fibers. We assume that the origin of the misinnervation was vagal, because the pupillary distortion could be elicited only by drinking, when permanent, significant esophageal peristalsis is required; but not by lower swallowing frequency (eating) and low volume load (saliva) at the same swallowing frequency as when the child was drinking. That is, the pupillary distortion was elicited mainly by the voluntary sequence of the swallowing act, which requires activity of the hypoglossal and glossopharyngeal nerves.