Because many eye movement disorders have a neural basis, the clinician should attempt to localize the potential lesion that might be producing the patient’s eye movement disorder. Anatomical localization will dictate patient evaluation, including imaging modality and differential diagnosis. It is also useful to conceptualize the anatomical pathway of the ocular motor system (ie, extraocular muscles, neuromuscular junction, orbit, CNs, brainstem, premotor input, and cerebrum) that is assumed to be involved (Fig 7-4). Adopting this kind of “wiring diagram” approach takes into account the supranuclear, internuclear, nuclear, and fascicular pathways within the brainstem, which then traverse the subarachnoid space, cavernous sinus, superior orbital fissure, and orbit, ending in the neuromuscular junctions of the extraocular muscles. In general, a lesion involving the CN nucleus or fascicle will cause neurologic deficits in addition to ophthalmoparesis (discussed later in the chapter). Central lesions can produce a clinically isolated CN III, IV, or VI palsy, but such isolated cranial neuropathies are the exception.
Figure 7-4 Anatomical substrate for localizing lesions of the infranuclear ocular motor pathways. This schematic provides a lateral view of CNs III, IV, and VI from the brainstem nuclei to the orbit. A sequential consideration of these pathways could begin either within the brainstem or within the orbit. The cranial nerve segments within the brainstem are often referred to as being “intramedullary.” The subarachnoid space lies between the brainstem and cavernous sinus. CN III exits the midbrain anteriorly, crosses near the junction of the internal carotid and posterior communicating arteries in the subarachnoid space, and enters the cavernous sinus, where it runs in the lateral wall. CN IV exits the midbrain posteriorly and crosses to the opposite side. It then courses through the subarachnoid space and into the cavernous sinus. CN VI exits the pons anteriorly, ascends along the clivus, crosses the petrous apex, and passes below the petroclinoid ligament to enter the cavernous sinus, where it runs between the lateral wall and the carotid artery.
(Used with permission from Yanoff M, Duker JS, eds. Ophthalmology. 2nd ed. St Louis: Mosby; 2004:1324, fig 199-1.)
Attempts at neural localization may fail or give false results in the presence of diffuse disease (eg, meningeal inflammation, as in sarcoidosis). In addition, this approach is not helpful in a clinical syndrome, such as Wernicke encephalopathy, in which imaging may not show characteristic structural disturbances.
Excerpted from BCSC 2020-2021 series: Section 5 - Neuro-Ophthalmology. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.