Horner syndrome (miosis, ptosis, and anhidrosis) is secondary to loss of ocular sympathetic innervation. Ptosis is less than 2 mm, the result of paralysis of Müller muscle, innervated by the sympathetic pathway. Anhidrosis is often not apparent to patients or clinicians. A pupillary finding specific in Horner syndrome is dilation lag. Because the dilator muscle is weak, the pupil dilates more slowly than the normal pupil.
This loss of ocular sympathetic innervation can be produced by a lesion anywhere along a three-neuron sympathetic pathway, from the hypothalamus down through the brain stem to the cervical cord, in the apex of the chest, along the carotid sheath, and in the cavernous sinus or orbit. Isolated Horner syndrome presenting with head or neck pain suggests an internal carotid artery dissection.
Management and Disposition
Associated signs and symptoms help direct the ED workup. A patient with cranial nerve abnormalities requires CT or MRI imaging and admission. In the setting of cervical spine trauma, neck immobilization and appropriate imaging studies are instituted. Consider carotid artery dissection in neck pain without trauma.
Classic signs of a Horner syndrome include meiosis and mild ptosis. Anhidrosis is less readily appreciated, and occurs with first- or second-order lesions only.
Miosis and dilation lag are accentuated in a darkened room.
A Pancoast tumor usually is caused by bronchogenic carcinoma and may present, as its presenting sign, as a Horner syndrome.
Cluster headaches, with autonomic sympathetic system dysfunction, are capable of producing an ipsilateral Horner syndrome.
Ipsilateral extraocular paresis, especially a 6th-nerve palsy, without other brain stem signs localizes pathology to within the cavernous sinus.
Horner Syndrome. Unilateral meiosis and ptosis are seen in this patient with Horner syndrome and sarcoma metastatic to the spine. (Photo contributor: Frank Birinyi, MD.)