Localization
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.
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.