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.
TadasukeTominaga, Yasuo Aihara, Takakazu Kawamata and Koji Arai
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