After using Hydroxyamphetamine 1%, a patient fails to dilate when assessed for Horner's syndrome. What is the most likely etiology?

In the context of Horner's syndrome, Hydroxyamphetamine is utilized to differentiate between preganglionic and postganglionic lesions causing the syndrome. When Hydroxyamphetamine is administered, it releases stored norepinephrine in the postganglionic neuron. If there is a functional postganglionic neuron, the pupil should dilate. The failure to dilate after using Hydroxyamphetamine suggests a postganglionic lesion, which points to issues occurring somewhere along the pathway from the sympathetic root to the target tissue.

Cervical sympathetic disruption can occur in several conditions, with carotid dissection being a notable cause. Carotid dissection can lead to a postganglionic Horner's syndrome because it affects the sympathetic fibers traveling alongside the carotid artery. Thus, when Hydroxyamphetamine is used, there is a failure of dilation due to the impaired function of postganglionic sympathetic fibers.

Wallenburg's syndrome, a lateral medullary infarct, and dorsal midbrain syndrome, which is associated with specific types of midbrain lesions, do not typically cause the same pattern of sympathetic disruption resulting in Horner's outcomes after Hydroxyamphetamine application. Similarly, while a Pancoast tumor can lead to Horner