The authors present the case of a patient diagnosed with Horner syndrome using apraclonidine eye drops and advocate for the performance of a larger study of apraclonidine for this use. A number of reports have described the efficacy of apraclonidine testing for Horner syndrome, but debate remains over its sensitivity in the acute setting.
Horner syndrome diagnosis is typically confirmed with pharmacological eye drop testing, traditionally with cocaine but increasingly with apraclonidine. The current criterion for the diagnosis of Horner syndrome is a reversal of anisocoria after bilateral administration of topical apraclonidine.
In the case presented in this study, the authors observed a response to apraclonidine relatively soon after the onset of Horner syndrome due to traumatic internal carotid artery dissection. There was a decrease in anisocoria with apraclonidine indicating sympathetic supersensitivity, but no reversal of anisocoria. The exact time of onset of the disruption of sympathetic innervation was not clear. The onset of ocular symptoms three hours prior to presentation is suggestive, but the lesion may have occurred at any time prior to the traffic accident in which the patient was involved four days earlier.
Testing with cocaine, on the other hand, has limitations. In the normal eye, instillation of cocaine drops should produce an increase in pupil diameter, while in an eye with Horner syndrome, the pupil will fail to dilate. However, the normal control pupil (contralateral eye) may not dilate due to the relatively weak dilating effect of cocaine. There is the risk of a false-positive result if the affected pupil is incapable of dilating for another reason. And cocaine, as a controlled substance, is often difficult to obtain.
The authors note that there are some unsettled issues regarding the use of apraclonidine for diagnosing Horner syndrome. It has been reported that testing with apraclonidine has a similar sensitivity to cocaine, except in the acute setting before the disruption of the sympathetic supply has produced denervation supersensitivity. The exact time interval required for the development of sufficient supersensitivity to produce a positive apraclonidine test and whether this is different in various causes of Horner syndrome remains unknown, as does the response to apraclonidine in patients with partial lesions.
The authors conclude that while the usefulness of apraclonidine in diagnosing acute and chronic Horner syndrome has been clearly demonstrated, a larger study is required to determine its true sensitivity and specificity, as well as to identify confounding factors and redefine the criteria for positive testing. Such a study might lead to modifying criteria for a positive test and allow pharmacological diagnosis of Horner due to both complete and incomplete disruption of the oculosympathetic pathway.