Oculomotor dysfunction may be resulted from a number of causes, including Tolosa-Hunt syndrome, aneurysm, microvascular ischemia, neoplasm and diabetic ophthalmoplegia [1, 4]. Identification of different etiologies is very important for subsequent treatment. Midbrain stroke mimicking oculomotor nerve palsy has been reported only rarely [2, 4]. In this report, we present a case of isolated unilateral oculomotor dysfunction caused by midbrain infarction.
Oculomotor nerve is the third cranial nerve that, together with the fourth and sixth cranial nerves, controls the eye movement. It contains fibers that innervate extraocular muscles of superior rectus, medial rectus, inferior rectus, and inferior oblique. Levator palpebrae superioris and pupillary sphincter are also included in oculomotor fascicles. These fascicles arise from different subnuclei, which are relatively dispersed, in the midbrain. Then, the fibers converge on the ventral side, and leave the brainstem between superior cerebellar and posterior cerebral arteries[5]. The oculomotor nerves course through many structures, such as red nucleus, cavernous sinus, cerebellar tentorium and superior orbital fissure. Any lesion along this path may result in a different forms of oculomotor nerve palsy [6, 7]. It is worth noting that parasympathetic fibers are thought to join the oculomotor nerve later and are located on the surface, whereas somatic fibers are located in the inner part of the nerve. Therefore, ischemic lesions such as diabetic neuropathy primarily affect the nerve's core, which is supplied by vasa vasorum, with sparing of the pupillary reflex, while compressive lesions such as aneurysms often affect pupillary reflex due to the damage from external structure [1]. In our patient, the isolated unilateral partial oculomotor paresis was due to the ischemic stroke in the paramedian area of the midbrain.
Oculomotor paralysis caused by midbrain infarction may be nuclear or subnuclear. Patients with nuclear oculomotor paralysis usually manifest as bilateral ptosis, restricted upward movement of the contralateral eye, and restricted downward and inward movement of the ipsilateral eye [8, 9]. Subnuclear oculomotor palsy usually only affects the ipsilateral eye. Patient's symptoms depend on the involvement of fibers from different subnuclei. The exact arrangement of fascicles arising from different oculomotor subnuclei is still unclear, although some hypotheses have been proposed [10, 11]. Our patient with paramedian midbrain infarction manifested as oculomotor nerve palsy with pupillary sphincter and inferior rectus muscles spared. We believe that fibers from Edinger-Westphal nucleus and inferior rectus nucleus do not course through this region (Figure 4). Consistent with our findings, a previous study in 5 patients with pure paramedian midbrain infarction demonstrated that oculomotor fascicles innervating the pupillary sphincter and inferior rectus muscles are relatively resistant to ischemia here [2].
In summary, we herein report a patient of isolated unilateral partial oculomotor paresis caused by pure midbrain infarction, whose pupillary sphincter and inferior rectus muscle were selectively spared. Our report adds to the understanding of fascicles arrangement in the midbrain.