Acute Painful Horner Syndrome as the First Presenting Sign of Carotid Artery Dissection
Background: Horner syndrome is a rare neurologic disorder that can arise from severe neurologic and systemic conditions, which may require immediate diagnosis with radiologic imaging and treatment with antiplatelet and anticoagulant therapy. Horner syndrome is often asymptomatic but can have distinct, easily identified characteristics seen with an ophthalmic examination.
Case Presentation: A 61-year-old woman presented with periorbital pain localized around and behind the right eye that she rated as 7 on a 10-point scale with onset 3 days prior. She reported light sensitivity, syncope, dizziness, and a recent history of transient ischemic attacks of unknown etiology. The patient had acute, slight ptosis with pathologic miosis and pain in the ipsilateral eye with no reports of exposure to miotic pharmaceutical agents and no history of trauma to the globe or orbit eliminated other differentials, leading to a diagnosis of right-sided Horner syndrome. She was referred for emergency department evaluation where radiography was indicative of an internal carotid artery dissection.
Conclusions: Due to possible life-threatening complications that can arise in patients with Horner syndrome, clinicians must have a thorough understanding of the condition, appropriate treatment, and management modalities. Determining the underlying etiology of Horner syndrome can help prevent a decrease in a patient’s vision or quality of life and in some cases prevent death. Magnetic resonance imaging and computed tomography should be used to rule out carotid artery dissection and other severe conditions.
Pathologic Mydriasis
Pathologic mydriatic pupils can result from dysfunction in the parasympathetic nervous system, which results in a pupil that is not sufficiently able to dilate with the removal of a light stimulus. Mydriatic pupils can be related to Adie tonic pupil, Argyll-Robertson pupil, third nerve palsy, trauma, surgeries, or pharmacologic mydriasis.2 The conditions that cause mydriasis can be readily differentiated from one another based on clinical examination.
Adie tonic pupil results from damage to the ciliary ganglion.2 While pupillary constriction in response to light will be absent or sluggish in an Adie pupil, the patient will have an intact but sluggish accommodative pupillary response; therefore, the pupil will still constrict with accommodation and convergence to focus on near objects, although slowly. This is known as light-near dissociation.2
Argyll-Robertson pupils are caused by damage to the Edinger-Westphal nucleus in the rostral midbrain.3 Lesions to this area of the brain are typically associated with neurosyphilis but also can be a result of Lyme disease, multiple sclerosis, encephalitis, neurosarcoidosis, herpes zoster, diabetes mellitus, and chronic alcohol misuse.3 Argyll Robertson pupils can appear very similar to a tonic pupil in that this condition will also have a dilated pupil and light-near dissociation.3 These pupils will differ in that they also tend to have an irregular shape (dyscoria), and the pupils will constrict briskly when focusing on near objects and dilate briskly when focusing on distant objects, not sluggishly, as in Adie tonic pupil.3
Mydriasis due to a third nerve palsy will present with ptosis and extraocular muscle dysfunction (including deficits to the superior rectus, medial rectus, inferior oblique, and inferior rectus), with the classic presentation of a completed palsy with the eye positioned “down and out” or the patient’s inability to look medially and superiorly with the affected eye.2
As in cases of pathologic mydriasis, a thorough and in-depth history can help determine traumatic, surgical and pharmacologic etiologies of a mydriatic pupil. It should be determined whether the patient has had any previous trauma or surgeries to the eye or has been in contact with any of the following: acetylcholine receptor antagonists (atropine, scopolamine, homatropine, cyclopentolate, and tropicamide), motion sickness patches (scopolamine), nasal vasoconstrictors, glycopyrrolate deodorants, and/or various plants (Jimson weed or plants belonging to the digitalis family, such as foxglove).2
