Abstract

Horner’s syndrome is characterized by the association of upper blepharoptosis with ipsilateral pupillary constriction, or miosis. Although controversy exists about who first described this condition, Horner’s syndrome is named for the Swiss ophthalmologist who reported a case in 1869.’ Disruption of sympathetic outflow to the head resulting in Horner’s syndrome may arise from damage at any level in the three-neuron pathway from the hypothalamus to the head and face. First-order, or central, lesions occur between the origin of the sympathetic pathway in the hypothalamus and its termination in the lower cervical and upper thoracic ciliospinal center of Budge and Waller. Tumors, infarctions, trauma, multiple sclerosis, and other conditions affecting the central nervous system may cause damage to first-order sympathetic neurons.“’ Second-order, or preganglionic, lesions occur between the first synapse in the ciliospinal center and the second synapse in the superior cervical ganglion. Responsible causes are usually tumors, as well as nonsurgical and surgical trauma. Apical bronchogenic carcinoma-termed Pancoast tumor-is one well-known cause of second-order Horner’s syndrome cases.’ Many cases of congenital Horner’s syndrome, which include iris heterochromia, are second-order cases and result from forceps injury in the region of the brachial plexus and lower neck at the time of delivery.‘,* Third-order, or postganglionic, lesions are caused by damage to the superior cervical ganglion or to sympathetic fibers distal to it. Thrombotic or atherosclerotic internal carotid disease, cavernous sinus lesions, tumors, cervical or facial trauma,

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