Horner syndrome: A new hypothesis for signaling pathway of enophthalmos sign

Horner syndrome (HS) is a neurological or/and neurosurgical disorder characterized by common signs including miosis, ptosis, anhidrosis, and enophthalmos. Enophthalmos is abnormally posterior displacement of the globe due to degradation of orbital fat, or loss of function of the orbitalis muscle. The main landmark for its diagnosis is a difference of 2 mm or more in the anteroposterior (AP) axis between the two globes.1 Enophthalmos manifests in two congenital or acquired forms that can result from anatomical or physiological changes especially HS.2 It occurs as a result of damage to the carotid artery, superior cervical ganglion (SCG) sympathectomy, inflammatory diseases, drug abuse, and neurocristopathy (abnormal migration of neural crest cells).2 The smooth muscle of the upper eyelid (Muller's muscle) is innervated by the surrounding plexus of internal carotid artery, but the smooth muscle of the lower eyelid (Kakizaki's muscle) that is not a single muscle is innervated by the surrounding plexus of external carotid artery. Moreover, the Lockwood's ligament is isolated by a layer of fat or is united to the capsulopalpebral fascia (CPF) between the inferior tarsal muscle, and the CPF is innervated by the surrounding plexus of external carotid artery.3 Signaling and new concept Therefore, any damage to this sympathetic (as a result of superior cervical ganglion sympathectomy) causes dysfunction of the lower eyelid components, including the CPF and its surrounding smooth muscle fibers, and finally leads to forward displacement of the lower eyelid as well as manifestation of the enophthalmos symptom.