Due to the separation of the third nerve fascicles as they leave their nuclear complex, pass through the red nucleus, substantia nigra, and the pyramidal tracts to exit the brainstem into the interpeduncular fossa, damage in this region often results in incomplete paralysis. The pupil may be spared, or an isolated paralysis of elevation may be found. Even patterns of isolated superior or inferior divisional palsies of the third nerve can arise from disease located within the midbrain. Associated deficits of additional midbrain structures are likely to be found, including vertical gaze pareses (damage to the rostral interstitial nucleus of the medial longitudinal fasciculus), bilateral ptosis (typically present with lesions of the third nerve nucleus), paralysis of convergence and/or accommodation, and loss of all contralateral somatic sensation . Most fascicular pareses are ischemic in origin, and are only occasionally the result of infiltrating of inflammatory processes. Microvascular ischemia of the oculomotor nerve arises from small-vessel disease of the vasa vasorum supplying the third nerve. It is the most common cause of oculomotor paresis in most ophthalmic practices. Though not specific, the presentation is characteristic, including acute onset of diplopia, complete or partial palsies of the muscles supplied by the third nerve, sparing of the pupillary sphincter, and ipsilateral retrobulbar and/or temporal pain. The pain is thought to stem from the acute inflammatory response to the infarcted nerve within the subarachnoid space, i.e., a locus of sterile meningitis. The pupillary sparing reflects the surface location of the autonomic fibers, providing some oxygen supply via the cerebral spinal fluid. The fibers are also small and have lower metabolic requirements than the larger, more quickly conducting oculomotor fibers. It also explains their greater susceptibility to compressive lesions Simultaneous damage to the sympathetic fibers in the cavernous sinus can also conceal damage done to the pupillomotor fibers by minimizing the resultant mydriasis. Vasculopathic oculomotor cranial nerve palsies are most common in middle-aged and elderly patients. The paresis is monocular, and typically, other cranial nerves are not affected. A spontaneous recovery is the rule, taking 4 to 6 months for completion. The diagnosis can initially be difficult. During the first 10 days, there may be a staircase progression of additional motor loss, which happens in more than half of all cases. Risk factors for this type of small-vessel disease include age, diabetes mellitus, hypertension, and generalized arteriosclerosis. Relapses in the same or other ocular motor nerves are not uncommon. More than one nerve can be involved at the same time and problems can appear bilaterally, but these are uncommon events. The diagnosis is difficult to confirm initially, but it is ultimately proven by the subsequent recovery.