LAUSR

H orner syndrome is characterized by the presence of a lesion at any location along the oculosympathetic pathway. It is clinically characterized by ipsilateral pupillary miosis, facial anhidrosis, ipsilateral upper eyelid ptosis, and mild lower eyelid elevation. The course of sympathetic fibers destined for Muller’s muscle in the upper eyelid is divided into first-, second-, and third-order segments. After leaving the area of the innominate artery on the right and the subclavian artery on the left just above the lung apex (around the level of the first and second thoracic spinal cord segments, T1/T2), postsynaptic second-order fibers pass through the inferior and middle cervical ganglia to terminate in the superior cervical ganglion at the level of the angle of the jaw (cervical spinal cord level C2) and carotid artery bifurcation. Postganglionic third-order fibers then ascend superiorly in the wall of the bifurcated carotid arteries, continue along the internal carotid artery (ICA) entering the cranium through the carotid canal into the cavernous sinus. Here, fibers leave the ICA to join the oculomotor nerve and course forward with the superior division of the oculomotor nerve as it passes through the orbital apex. The fibers then reach their final destination to innervate Muller’s muscle. This muscle provides 1–3 mm of upper eyelid elevation (1). The use of selective alpha-2 agonists for improvement of Muller’s muscle-related ptosis has been reported in the past with the use of apraclonidine (2,3). It is believed that, due to its mechanism of action, brimonidine cannot have this same effect as apraclonidine. However, here, we present a case of Horner syndrome– induced ptosis after anterior laminectomy; the signs improved with the instillation of brimonidine tartrate.