![]() Direct central causes include bleeding into midbrain parenchyma or direct pressure of a large basilar artery on the nucleus. Direct peripheral causes include, 1) local pressure by the aneurysm, and 2) hemorrhagic dissection of the nerve. A single case of an AComA aneurysm rupture in which bilateral oculomotor nerve palsy was presented was reported by Coyne and Wallace ( 4).Ī number of mechanisms of a third nerve palsy in patients with an intracranial aneurysm have been classified by Fox ( 5). In another expired patient, a remarkable descent of the terminal portion of the basilar artery was found, indicating downward axial displacement of the midbrain by supratentorial hypertension, resulting in total ophthalmoplegia. They explained in patient with A1 aneurysm and megadolichobasilar anomaly that the oculomotor nerve might be more easily displaced or squeezed between the posterior cerebral and superior cerebellar arteries by increased ICP. These patients had A1 and AComA aneurysms and were presented with unilateral partial cranial nerve III palsy and bilateral total ophthalmoplegia, respectively. Suzuki and Iwabuchi ( 3) recorded false localizing third cranial nerve palsy in two patients with ruptured aneurysms. However, she complained of diplopia and slightly decreased vision.īilateral 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 vicinity of the oculomotor nerve. Also, both of her ophthalmoplegia recovered partially, resulting in intermittent spontaneous eye opening, lateral deviation in the right eye, centrally fixed pupil in the left eye, and both isocoric and reactive pupil ( Fig. The final examination performed in one year showed that the patient communicated well with simple words, and that the left arm and leg remained at grade 4+ and the right side at grade 4. Three months after surgery, follow-up magnetic resonance imaging (MRI) demonstrated infarction of left medial occipital lobe and lacunar infarction of the pons ( Fig. At this point, the author came to recognize these events and finally confirmed external ophthalmoplegia of the right eye and complete ophthalmoplegia of the left eye. There were still limitations of ocular movements of both eyes.Ī digital subtraction angiogram reveals a saccular aneurysm on the anterior communicating artery.Īs her consciousness began to improve slowly after shunting over a period of weeks, it was noted that she was unable to open her both eyes, indicating bilateral ptosis. Her left pupil decreased to 3 mm in size but did not react to direct or indirect light. Twenty days later, ventriculo-peritoneal shunting was done due to communicating hydrocephalus. The ventricular catheter was removed on the 14th postoperative day when it was still measured at 25 mm Hg. Thereafter, the right pupil gradually decreased (2 mm) and reacted to light but the left one was still dilated without direct or indirect light reflex, in which pupil size changed a little in accordance with intermittent ventricular drainage. Follow-up CT scan showed no significant change. On the 5th postoperative day, both pupils were dilated (6 mm) with sudden elevation of ICP to 50 mm Hg during temporary closure of ventricular catheter. No additional neurological deficits were observed postoperatively. The aneurysm could be safely dissected and was successfully clipped. After opening the Sylvian fissure, it was observed that the basal cistern was obstructed with clot. The patient underwent an operation on the next day via left pterional approach. A digital subtraction angiogram revealed a saccular aneurysm on the AComA ( Fig. Seven hours after EVD, the right pupil became reactive to light, but left pupil was nonreactive to light with 4 mm in size. Initial intracranial pressure (ICP) was 45 mm Hg, and subsequently, the pressure remained between 15 and 25 mm Hg after intermittent cerebrospinal fluid (CSF) drainage. Emergency extraventricular drainage (EVD) was performed. Computed tomographic (CT) scanning demonstrated extensive subarachnoid hemorrhage spreading around the both Sylvian, basal, and interhemispheric cistern ( Fig. Both pupils appeared centrally fixed, dilated (6 mm), and nonreactive to direct or indirect light stimuli. On neurological examination, she was semicomatose with flexion to painful stimulation. There was no history of diabetes mellitus, hypertension, heart disease, stroke, or cancer. Pulse rate and blood pressure were 68 beats per minute and 130/80 mm Hg, respectively. ![]() A 68-yr-old female was found unconscious. ![]()
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