Figure 187.1.— Oculosympathetic pathway is represented as a blue line. The pathway originates in the posterior hypothalamus; from there it travels ipsilaterally to the Budge ciliospinal center; from the Budge ciliospinal center it travels to the superior cervical ganglion; from the superior cervical ganglion it enters the skull and then the orbit. The facial sympathetic pathway takes a similar path until the superior cervical ganglion; from the superior cervical it travels with the external carotid artery.
Oculosympathetic pathway damage produces Horner syndrome. The manifestations of Horner syndrome are ptosis, miosis, and anhydrosis. Brainstem lesions involve the central sympathetic tract and produce anhydrosis involving the face and body. The pathology of a brainstem lesion is usually not found. Lesions in the brachial plexus (Figure 187.1 [A]) are more common than brainstem lesions. They involve the cervico-thoracic sympathetic trunk. These lesions occur either at C8, T1, or T2 ventral roots or spinal nerves. Anhydrosis only involves the face. Horner syndrome due to brachial plexus injury results from trauma, but may also occur with congenital chickenpox or with involvement outside of the brachial plexus in the thoracic spine. Horner syndrome is usually associated with Klumpke palsy. Horner syndrome may also occur with congenital neuroblastomas. The cause of Horner syndrome is often not found. Neonates with Horner syndrome without an obvious cause should have an MRI of the brain and neck, and blood studies searching for the possibility of excessive catecholamine secretion.