Abstract
Oculomotor nerve palsy has been recognized as a localizing sign due to aneurysms along the internal carotid artery, resulting from direct pressure on the nerve. There were only two case reports of an anterior communicating artery (AcomA) aneurysm rupture followed by bilateral oculomotor nerve palsy. We experienced the rare finding of a patient with transient bilateral oculomotor nerve palsy unrelated to consciousness disturbance that started about 38 hours after subarachnoid hemorrhage (SAH) due to AcomA aneurysm rupture. Without raised intracranial pressure, bilateral mydriasis resolved spontaneously 22 hours later. A thick clot Fisher group 3 SAH occupying perimesencephalic, interhemispheric, and sylvian cisterns bilaterally,remained in CT scans afterthe operation. Reconstructed MRI data of the oculomotor nerve were converted to a curved multiplanar reconstruction (MPR) image suggested that subarachnoid blood occupying the perimesencephalic cisterns bilaterally induced compression on the oculomotor nerves directly, and the subsequent local edema caused transient bilateral palsy.
Highlights
Unilateral oculomotor nerve palsy has been recognized as a localizing sign due to aneurysms along the internal carotid artery, at the internal carotid-posterior communicating artery (ICA-PcomA) junction and is considered to be a variable symptom caused by direct pressure on the nerve
In this report we describe the rare finding of a patient with transient bilateral oculomotor nerve palsy unrelated to consciousness disturbance that started about 38 hours after subarachnoid hemorrhage due to anterior communicating artery (AcomA) aneurysm rupture
We reviewed and discussed the possible mechanisms of this phenomenon related to an AcomA aneurysm rupture
Summary
Unilateral oculomotor nerve palsy has been recognized as a localizing sign due to aneurysms along the internal carotid artery, at the internal carotid-posterior communicating artery (ICA-PcomA) junction and is considered to be a variable symptom caused by direct pressure on the nerve. About 46 hours after the onset, pupillary size was at the maximum (Figure 2A) Both eyes were abducted, and the findings were considered to be isolated bilateral oculomotor nerve palsy (Figure 2B). The findings were considered to be isolated bilateral oculomotor nerve palsy (Figure 2B) During these clinical developments, his consciousness level and clinical condition remained unchanged – GCS 8 (E2VtM5). Direct and indirect reflexes to light returned soon after Both pupillary sizes were back to normal 22 hours after the onset of the bilateral oculomotor nerve palsies. B:About 46 hours after the onset, both pupilsdilatation was at their maximum and both eyes were abducted as shown on the figure It indicated bilateral isolated oculomotor nerve palsy. FwFighiugicruherse5h:o5MwPsRvMthiiemePwRatr)gaiemwctohaofgifhcetehhaoesdfhrMhiogewRhaItsd(oAtcM:huaelxRoiamItrl(oavAtcie:otawrxon)ifaealrtnvhvdeiee(.BwCr:i:sg)aThaghtniettdopacal(uBtvhli:oewswmaag)yoitottofarl trheceonnesrtvruecwtiaosnnea(uMrvtoPemR. )Cai:tmiTcaahgleleypcoanthvwerateydotfotahecunrveerdvemwulatispalauntaormatically converted to a curved multiplanar reconstruction (MPR) image. © Under License of Creative Commons Attribution 3.0 License
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