Aneurysm Causing Bilateral Oculomotor Nerve Palsy 175 Fig. 4. Postoperative photograph by one year follow-up shows lateral deviation in the right eye, centrally fixed pupil in the left eye, and both isocoric and reactive pupils. ined at grade 4+ and the right side at grade 4. Also, both of her ophthalmoplegia recovered partially, resulting in inter- mittent spontaneous eye opening, lateral deviation in the right eye, centrally fixed pupil in the left eye, and both iso- coric and reactive pupil (Fig. 4). However, she complained of diplopia and slightly decreased vision. DISCUSSION Bilateral third cranial nerve palsy as a false localizing sign due to a ruptured anterior communicating artery aneurysm is very rare because AComA aneurysms are not in the vicin- ity of the oculomotor nerve. Suzuki and Iwabuchi (3) recorded false localizing third cranial nerve palsy in two patients with ruptured aneurysms. These patients had A1 and AComA aneurysms and were presented with unilateral partial cranial nerve III palsy and bilateral total ophthalmoplegia, respective- ly. They explained in patient with A1 aneurysm and mega- dolichobasilar anomaly that the oculomotor nerve might be more easily displaced or squeezed between the posterior cere- bral and superior cerebellar arteries by increased ICP. In ano- ther expired patient, a remarkable descent of the terminal portion of the basilar artery was found, indicating downward axial displacement of the midbrain by supratentorial hyper- tension, resulting in total ophthalmoplegia. A single case of an AComA aneurysm rupture in which bilateral oculomotor nerve palsy was presented was reported by Coyne and Wal- lace (4). A number of mechanisms of a third nerve palsy in patients with an intracranial aneurysm have been classified by Fox (5). Direct peripheral causes include, 1) local pressure by the ane- urysm, and 2) hemorrhagic dissection of the nerve. Direct cen- tral causes include bleeding into midbrain parenchyma or direct pressure of a large basilar artery on the nucleus. Indi- rect peripheral causes include increased ICP (from clot, edema, hydrocephalus) causing uncal herniation. Indirect central causes include increased ICP and vasospasm (6). The case of Coyne and Wallace (4) showed close similarity to the present case with respect to the pathogenesis but a little difference from clinical signs and course of the bilateral oculomotor nerve palsy. In their report, raised ICP without brain herni- ation and compression of the third nerves within the perimes- encephalic cisterns by focal subarachnoid clot were suggest- ed as possible underlying mechanisms of the palsies. When the peripheral oculomotor nerve is involved by an aneurysm, usually the pupilloconstricter fibers are involved first, followed by palsy of the levator palpebrae, superior rec- tus, and medial rectus, in order. In contrast, when there is an intramedullary lesion, the pupilloconstricter fibers can be saved (7, 8). While the phenomenon of a pupil-sparing ocu- lomotor nerve palsy caused by an aneurysm has been well documented, it is nonetheless an uncommon event (9-11). In diabetes, a pupil-sparing oculomotor nerve palsy leads to loss of myelin and axons within that central portion, but may spare the peripheral regions where pupillary fibers travel (12). In the present patient, it is likely that the microvascular sup- ply to the inner nerve fibers of right third nerve was compro- mised while more peripheral fibers still received an adequate vascular supply. It is clinically difficult to ascertain the exact pathophysio- logic mechanism responsible for the present case. This nerve injury might be caused by 1) direct compression of the nerve derived from the extensive clot in the basal cistern, 2) uncal herniation, 3) remote effect due to increased ICP, and less likely, 4) vasospasm of branches of basilar artery. In the present pa- tient, these several features typically seen in other reports were found to be co-existing. The development of infarction of left medial occipital lobe usually signifies incipient uncal herni- ation. Most likely, brain herniation, along with dense hem- orrhage and increased ICP, is a mechanism of the left oculo- motor nerve palsy. However, relatively good improvement of this patient’s neurological deficits and the absence of mid- brain and uncal lesion on MRI suggest that focal vasospasm is one rare possibility of infarction of this medial occipital lobe and lacunar infarction of the pons. In contrast, the remote effect due to increased ICP could conceivably account for pupillary change of the right eye according to ventricular drainage. Eye opening on command or painful stimulus is most sig- nificant within the first 72 hr following an injury. After this time, even patients who will remain vegetative may open their eyes spontaneously. Delay in the diagnosis of this condition after surgery could be common because of lack of recognition of ptosis in an unconscious patient. Despite considerable variety in the degree of recovery, many patients show little functional impairment. However, this relates to the nature of the hemorrhagic insult. It seems to be possible that early operative decompression of the cistern and direct neck clipping are the therapeutic maneuvers most