- Department of Neurosurgery, PGIMER, Chandigarh, India
- Department of Neuroradiology, PGIMER, Chandigarh, India
Department of Neuroradiology, PGIMER, Chandigarh, India
DOI:10.4103/2152-7806.153877Copyright: © 2015 Srinivasan A. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
How to cite this article: Srinivasan A, Dhandapani S, Kumar A. Pupil sparing oculomotor nerve paresis after anterior communicating artery aneurysm rupture: False localizing sign or acute microvascular ischemia?. Surg Neurol Int 24-Mar-2015;6:46
How to cite this URL: Srinivasan A, Dhandapani S, Kumar A. Pupil sparing oculomotor nerve paresis after anterior communicating artery aneurysm rupture: False localizing sign or acute microvascular ischemia?. Surg Neurol Int 24-Mar-2015;6:46. Available from: http://sni.wpengine.com/surgicalint_articles/pupil-sparing-oculomotor-nerve-paresis-anterior-communicating-artery-aneurysm-rupture-false-localizing-sign-acute-microvascular-ischemia/
Background:We describe a rare case of solitary pupil sparing oculomotor nerve paresis following rupture of anterior communicating artery (ACom) aneurysm and discuss the pertinent literature. Oculomotor nerve paresis caused by an ACom aneurysm rupture is an uncommon occurrence. Also, partial paresis affecting only fibers of superior division of oculomotor nerve is never reported before.
Case Description:A 55-year-old female, known hypertensive presented 5 days after an episode of acute severe headache, with Glasgow Coma Scale (GCS) of E2V2M5, left ptosis, normal pupils, paraparesis, and computed tomography (CT) scan showed diffuse subarachnoid hemorrhage (SAH). CT angiography revealed ACom aneurysm pointing antero-superiorly toward right. Patient later underwent endovascular coiling of the aneurysm. Subsequently there was partial improvement of ptosis in 3 weeks.
Conclusion:Though pupil sparing oculomotor nerve paresis may not have much localizing value, it helps to understand acute microvascular spasm with potential therapeutic implications.
Oculomotor nerve paresis associated with subarachnoid hemorrhage is typical of aneurysms located at the junction of the internal carotid artery and posterior communicating artery (PCom), intracavernous part of the internal carotid artery, basilar artery, posterior cerebral artery, and superior cerebellar artery. However, oculomotor nerve paresis caused by an anterior communicating artery (ACom) aneurysm is a very uncommon occurrence. More importantly, partial paresis affecting only the fibers of superior division of third cranial nerve (CN) has never been reported before. Management and the pertinent literature are reviewed along with the probable mechanism of nerve involvement.
A 55-year-old female, known hypertensive presented 5 days after an episode of acute severe headache, with Glasgow Coma Scale (GCS) of E2V2M5, left ptosis, normal pupils [
Paresis of CN III is associated with ruptured aneurysms in 30% of patients.[
Although there has been six cases of CN III paresis associated with ACom aneurysms,[
The CN III nucleus comprises a complex of subnuclei located within the midbrain, ventral to the periaqueductal gray matter. The motor neurons of each subnuclei innervate their corresponding ipsilateral extraocular muscles except for the superior rectus subnuclei, which innervate the contralateral superior rectus muscle, and the midline levator palpebrae subnuclei, which innervate the ipsilateral and contralateral levator palpebrae muscles.[
The nerve exits the midbrain just medial to the cerebral peduncle as 10 to 15 rootlets merging to form a single nerve, and then it passes between the posterior cerebral and superior cerebellar arteries, traveling adjacent to as well as inferior and lateral to the PCom to arrive at the superolateral aspect of the cavernous sinus.[
Ptosis can be present at birth (congenital) or develop later in life (acquired). Ptosis may be due to a myogenic, neurogenic, aponeurotic, mechanical, or traumatic cause. Usually, ptosis occurs isolated, but may be associated with various other conditions, like immunological, degenerative, or hereditary disorders, tumors, or infections. However, these etiologies cannot explain the ptosis, which presented as an acute event for the first time following SAH.
The likely role for the trigemino-oculomotor pathway is to provide inhibition of levator motor neurons during the down-phase of a blink elicited by trigeminal stimulation. However, this cannot explain unilateral ptosis and this has more significance in the corneal reflex physiology.[
Although the subarachnoid or cisternal portion of CN III is a single structure, based on previous clinical observations, there is a topographic arrangement of the fibers within the nerve but the precise anatomical arrangement in humans has not been specified. The few localization studies performed in animals have demonstrated pupillary fibers to be superficially located in the cisternal portion of CN III.[
Though pupil sparing CN III paresis may not have much localizing value, it helps to understand acute microvascular spasm with potential therapeutic implications.
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