Background: Brain aneurysms are mostly discovered during the investigation of subarachnoid hemorrhage (SAH). Some patients present neurological signs that may suggest the aneurysm’s topography, and the oculomotor nerve palsy (ONP) of the same side of the aneurysm is the most common sign. Only one case report of contralateral palsy was previously described in the medical literature. Case Description: Authors describe a patient who presented a classic manifestation of SAH associated with complete ONP, whose vascular investigation demonstrated a brain aneurysm located in the contralateral intracranial carotid. The patient was surgically treated with great neurologic outcome, and late angiography did not evidence other vascular abnormalities. Conclusion: The ipsilateral ONP is a common sign found in posterior communicating artery aneurysms; however, such aneurysm can have different presentations due to the elevation of intracranial pressure, and, in rarer cases, the ONP cannot be operated as a localizing sign

Almeida, Leandro Pelegrini de

Casarin, Mateus Carvalho

Finger, Guilherme

Martins, Otávio Garcia

Nesi, William Mazzucco

Santos, Samir Cezimbra dos

Schiavo, Felipe Lourenzon

Stefani, Marco Antonio

Surgical Neurology International

English

Universidade Federal do Rio Grande do Sul

Ruptured aneurysm in the posterior communicating segment of carotid artery presenting with contralateral oculomotor nerve palsy

Lume 5.8

Surgical Neurology International • 2019 • 10(177) | 1is is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-Share Alike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.©2019 Published by Scientific Scholar on behalf of Surgical Neurology InternationalCase ReportRuptured aneurysm in the posterior communicating segment of carotid artery presenting with contralateral oculomotor nerve palsyGuilherme Finger1,2, Otávio Garcia Martins3, William Mazzucco Nesi1, Mateus Carvalho Casarin1, Leandro Pelegrini de Almeida1, Felipe Lourenzon Schiavo1, Samir Cezimbra dos Santos1, Marco Antonio Stefani21Department of Neurosurgery, Cristo Redentor Hospital, 2Graduate Program in Surgical Sciences, Federal University of Rio Grande do Sul - Brazil, Porto Alegre, 3Department of Neurosurgery, Federal University of Pelotas, Pelotas, RS, Brazil. E-mail: Guilherme Finger - guilhermefingermd@gmail.com; *Otávio Garcia Martins - otvmartins@gmail.com; William Mazzucco Nesi - william.nesi@hotmail.com; Mateus Carvalho Casarin - mateusccasarin@gmail.com; Leandro Pelegrini de Almeida - leandropelegrini@yahoo.com.br; Felipe Lourenzon Schiavo - felipeschiavo@icloud.com; Samir Cezimbra dos Santos - samirdossantos@terra.com.br; Marco Antonio Stefani - marco@stefani.med.br*Corresponding author:Otávio Garcia Martins, Rua São Pedro 153, ap 902. Marechal Rondon Neighborhood, Canoas, RS 92020-480, Brazil.otvmartins@gmail.comReceived : 19 March 19 Accepted : 09 August 19 Published : 13 September 19DOI 10.25259/SNI_203_2019Quick Response Code:INTRODUCTIONSubarachnoid hemorrhage (SAH) is a condition characterized by the presence of blood in the subarachnoid space, whose origin may be secondary to arterial dissection, trauma, and venous or aneurysm rupture.[18] Among the nontraumatic SAH, aneurysm rupture is responsible for 85% of the cases and represents the most life-threatening etiology of SAH whose 30-day mortality can reach 50%, and 30% of the survivors have moderate-to-severe disability.[1,5,11] Mortality occurs secondary to complications of the primary bleeding, such as increased intracranial pressure (ICP), hydrocephalus, and late brain ischemia; or due to a rebleeding, if the aneurysm is not urgently treated.ABSTRACTBackground: Brain aneurysms are mostly discovered during the investigation of subarachnoid hemorrhage (SAH). Some patients present neurological signs that may suggest the aneurysm’s topography, and the oculomotor nerve palsy (ONP) of the same side of the aneurysm is the most common sign. Only one case report of contralateral palsy was previously described in the medical literature.Case Description: Authors describe a patient who presented a classic manifestation of SAH associated with complete ONP, whose vascular investigation demonstrated a brain aneurysm located in the contralateral intracranial carotid. e patient was surgically treated with great neurologic outcome, and late angiography did not evidence other vascular abnormalities.Conclusion: e ipsilateral ONP is a common sign found in posterior communicating artery aneurysms; however, such aneurysm can have different presentations due to the elevation of intracranial pressure, and, in rarer cases, the ONP cannot be operated as a localizing sign.Keywords: Brain aneurysm, Cranial mononeuropathy, Oculomotor nerve disease, Ruptured intracranial aneurysm, Subarachnoid hemorrhagewww.surgicalneurologyint.comSurgical Neurology InternationalEditor-in-Chief: Nancy E. Epstein, MD, NYU Winthrop Hospital, Mineola, NY, USA.SNI: Neurovascular Editor  Kazuhiro Hongo, MD  Shinsui University, Matsomoto, Japan Open Access Finger, et al.: Contralateral oculomotor nerve palsy by ruptured aneurysm in the posterior communicating segment of carotid arterySurgical Neurology International • 2019 • 10(177) | 2Oculomotor nerve palsy (ONP) is a classic localizing sign of aneurysms situated along its course, being the posterior communicant artery (PComA) or communicant segment of internal carotid artery (ICA), the main locations of aneurysms associated with ONP at the same side of the aneurysm.[4,8,19] e third nerve dysfunction usually results from a direct compression of the nerve by the aneurysm growth or rupture.[18] However, contralateral presentation represents a very rare clinical finding of this pathology[5,18]is case report describes the third case of ONP associated with contralateral ICA-PComA junction aneurysm,[15,17] but the second whose palsy was manifested at the acute scenario. e patient consented to publication of his image.CASE REPORTA 60-year-old male, with no previous medical comorbidity, woke up during the night with a severe sudden headache. e patient tried to get up from the bed when he lost consciousness. e patient could not determine how long he persisted unconscious, but when he recovered mental functions, he called for medical support (patient lives alone). According to the patient, since he recovered consciousness, he persisted with a painful headache noticing that he could not open his left eyelid. e urgent medical assistance team promptly forwarded the patient to a tertiary hospital. At emergency admission, the patient was conscious, interacting adequately with the physicians, mobilizing all members without motor or sensitive deficits, but presented a marked neck stiffness and positive Brudzinski’s sign. e patient presented a complete left eyelid ptosis, with divergent strabismus due to a lateral rotation of the left eyeball and anisocoria with the left pupil mydriasis. Ocular extrinsic movement of the right eyeball was preserved; however, the superior, inferior, and medial movement of the left eyeball was compromised [Figure 1], and the left pupil constriction due to light stimuli was absent (for both photomotor and consensual tests). e patient was immediately submitted to a computed tomography (CT) examination without contrast infusion, which showed SAH in the interpeduncular and ambient cisterns, interhemispheric and lateral fissures, and also in the fourth ventricle [Figure 2]. Once the diagnose of spontaneous SAH was established, the patient was submitted to arteriography of the brain vessels that showed an aneurysm of PComA segment of the right ICA, measuring 9 mm of length, 5 mm wide, and with a neck of 4 mm. No other aneurysms were identified. erefore, authors concluded that they were facing a patient with a ruptured aneurysm of the ICA-PComA junction, classified as Hunt-Hess 2 and CT Fisher scale of 4. e patient was submitted to surgical clipping of the aneurysm. e procedure was conducted without aneurysm bleeding or other surgical complications, and the patient returned to the intensive care unit (ICU) where he was managed according to the current protocols for the treatment of acute SAH. e patient presented a satisfactory clinical and neurologic recovery, without late ischemia, vasospasm, infections, or other systemic complications. e patient was released from the hospital with an excellent clinical condition harboring only the oculomotor palsy that he had partially recovered by the time of 6 months of follow-up.DISCUSSIONAneurysmal SAH usually presents unspecific symptoms such as severe headache, vomiting, and photophobia. ese symptoms, despite its importance to suspicion of SAH, do not allow the topographic diagnosis of the aneurysm. However, the presence of certain infrequent specific signs can suggest the aneurysm position, operating as localizing signs.[2,3] Examples of these signs are partial blindness by ICA-ophthalmic artery junction aneurysm,[14] ataxia and nystagmus by posterior circulation aneurysms,[3] and complete ONP by PComA aneurysms.[2,10]e oculomotor nerve emerges from the interpeduncular fossa in the midbrain, medially to the cerebral peduncles. At its point of emergence of the brainstem, it is closely related to the posterior cerebral artery (PCA) superiorly and superior cerebellar artery (SCA) inferiorly. Furthermore, the nerve Figure 1: Ocular extrinsic examination at hospital admission demonstrating complete left oculomotor nerve palsy. (a) Both eyelids closed. (b) Complete ptosis of the left eyelid. (c) e patient looking forward, demonstrating a left rotation of the left eyeball due to abducens nerve function not balanced by the oculomotor nerve stimuli over the medial rectus muscle. (d) e patient looking to the right, without medial movement of the left eyeball. (e) e patient looking upward without superior vertical movement of the left eyeball. (f) e patient looking downward without inferior vertical movement of the left eyeball.afb cd eFinger, et al.: Contralateral oculomotor nerve palsy by ruptured aneurysm in the posterior communicating segment of carotid arterySurgical Neurology International • 2019 • 10(177) | 3gets its vascular supply from the basilar system at this point. It passes inferomedial to the uncus and inferolateral to the PComA to enter the roof of the cavernous sinus (CS) through the oculomotor trigone. Up to this point, the nerve can be affected by several pathological processes such as tumors, clots in the interpeduncular cistern, and direct compression by aneurysms of the underlying arteries.[12]e cavernous segment of the oculomotor nerve runs through the lateral wall of the CS superiorly. e nerve enters on the CS passing through the oculomotor triangle, which is delimited by the anterior petroclinoid ligament, the posterior petroclinoid ligament, and the interclinoid ligament [Figure  3]. In addition, there is an entry point known as oculomotor porus and represents the main fixation point of the nerve. ese areas of attachment and narrowing of the nerve pathway could explain the high vulnerability during pathological conditions, which allow contusions against the dural (ligaments) and bone structures (petrous apex).[12]e ICA-PComA junction is the most common location of aneurysm that courses with ipsilateral ONP, with a prevalence of 34%–56% among ruptured cases.[16] However, due to the proximity with other arterial structures, the palsy can also be associated with aneurysm located at the ICA, SCA, PCA, basilar artery apex, and anterior choroidal artery. [4,8,19]In the aneurysm scenario, the main mechanism of ipsilateral ONP is related to the compression of the nerve fibers by the aneurysm itself, increased ICP with or without brain herniation, compression within the perimesencephalic cisterns by focal blood clot, or chemical lesion by the blood metabolites in subarachnoid space.[18] In the few reports of contralateral palsy in the acute SAH scenario, some theories to explain the remote contralateral deficit were proposed: one hypothesis consists in compression of nerve due to the increased ICP. All the cranial nerves can be affected by increased ICP with or without herniation syndromes,[13] and it cannot be excluded as a possible cause of the deficit in our patient. Other possibilities are oculomotor nerve compression by a subarachnoid blood clot within the perimesencephalic cistern and the lesion by the jet stream of blood from the aneurysm. In this scenario, the osmotic tonicity of the surrounding blood, the toxic effects of the concentrated blood breakdown products, and the ischemia by compression of the small feeding arterioles of the nerve can contribute.[6] Moreover, vasospasm of feeding arteries of the nerve is also a possible cause. However, the early onset of the palsy in our patient suggests that vasospasm, which typically occurs 4  days after SAH,[7,9] is less likely to be the etiology.Especially in this case, authors hypothesize that elevation of ICP may be more strongly pointed as the etiological factor of the contralateral ONP due to the establishment of the deficit in the ictus of the event. A  sudden elevation of ICP may compress the oculomotor nerve at its vulnerable points into the CS roof or in the oculomotor trigone.[12] Compression of the nerve by clots can also not be ruled out as hypothesis since there was a presence of hyperdense images in the perimesencephalic cistern in the CT [Figure 2].Somagawa et al. reported a similar case of an acute SAH of the ICA-PComA junction with contralateral ONP.[15] In this case, the patient was affected with neurogenic pulmonary edema due to spontaneous SAH. After 1  day on the ICU, the patient presented with rebleeding and the left ONP. Subsequent angiography revealed a right ICA-PComA aneurysm. e clinical finding was associated with a massive perimesencephalic hemorrhage on CT, which suggests that Figure  2: Computed tomography at hospital admission demonstrating subarachnoid hemorrhage on the interpeduncular and ambient cisterns, interhemispheric and lateral fissures, and also in the fourth ventricle.Figure 3: Entry of the oculomotor nerve into the cavernous sinus through the oculomotor triangle, which is a potential compression point. Structures of the oculomotor triangle are shown. ON -  Oculomotor nerve, BA -  Basilar artery, APCL -  Anterior petroclinoid ligament, PPCL -  Posterior petroclinoid ligament, ICL -  Interclinoid ligament. Courtesy of the Rhoton Collection, American Association of Neurological Surgeons/Neurosurgical Research and Education Foundation.Finger, et al.: Contralateral oculomotor nerve palsy by ruptured aneurysm in the posterior communicating segment of carotid arterySurgical Neurology International • 2019 • 10(177) | 4the compression by the clot or the jet stream could have been the cause of the contralateral nerve lesion. e properly treatment of the aneurysm with coiling did not improve the palsy deficit.[15]Another case reported was a patient of Sun et al., who presented a PComA-ICA junction aneurysm that was treated with clipping.[17] Preoperatively, a lumbar catheter was placed after anesthesia induction to facilitate intraoperative brain relaxation and postoperative drainage of bloody cerebrospinal fluid (CSF). On postoperative day 3, the patient developed a complete left ONP that was associated with CSF overdrainage by the lumbar catheter: a head CT showed collapsed cerebral cisterns and shifted midline structures. is could collectively push the oculomotor nerve to the tentorial notch, causing the palsy. In addition, the clipping of the catheter resulted in the total recovering from the ONP palsy 6 h later. Although it occurred in the acute SAH scenario, the contralateral ONP was associated with CSF overdrainage and not directly to the pathophysiological consequences of the presence of blood in the subarachnoid space.In our case, the definitive treatment of the aneurysm with clipping was not associated with early improvement; however, at 6 months of follow-up, he had partially recovered the nerve’s functions. e recovery from nerve palsy depends on the time between the onset of symptoms and surgery. e earlier the operation is done, the higher is the chance of nerve function recovery.[2,4,19] In addition, such recovery is less likely if the palsy is present for more than 10 days before surgery or if signs of recovery have not started within a few weeks after operation.[16,19]is case may demonstrate that ONP may behave as a nontopographic sign in cerebral aneurysmal disease, and advanced neuroimaging is required to determine the location of aneurysms in patients with SAH.CONCLUSIONContralateral ONP is an extremely rare symptom of ICA-PComA aneurysm with only two cases reported, including ours. e pathophysiology of this phenomenon may depend on several factors such as intracranial hypertension, the presence of clots in the subarachnoid space, or the toxic effect of blood metabolites. In cases of late contralateral ONP, other events such as vasospasm and rebleeding may also be associated.Declaration of patient consente authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. e patient understand that his names and initials will not be published and due efforts will be made to conceal his identity, but anonymity cannot be guaranteed.Financial support and sponsorshipNil.Conflicts of interestere are no conflicts of interest.REFERENCES1. Broderick JP, Brott T, Tomsick T, Miller R, Huster G. Intracerebral hemorrhage more than twice as common as subarachnoid hemorrhage. J Neurosurg 1993;78:188-91.2. Cianfoni A, Pravatà E, De Blasi R, Tschuor CS, Bonaldi G. Clinical presentation of cerebral aneurysms. Eur J Radiol 2013;82:1618-22.3. Edlow JA, Caplan LR. Avoiding pitfalls in the diagnosis of subarachnoid hemorrhage. N Engl J Med 2000;342:29-36.4. Fujiwara S, Fujii K, Nishio S, Matsushima T, Fukui M. Oculomotor nerve palsy in patients with cerebral aneurysms. Neurosurg Rev 1989;12:123-32.5. Hop JW, Rinkel GJ, Algra A, van Gijn J. Case-fatality rates and functional outcome after subarachnoid hemorrhage: A systematic review. Stroke 1997;28:660-4.6. Hoya K, Kirino T. Traumatic trochlear nerve palsy following minor occipital impact – four case reports. Neurol Med Chir (Tokyo) 2000;40:358-60.7. Kang SD. Ruptured anterior communicating artery aneurysm causing bilateral oculomotor nerve palsy: A  case report. J Korean Med Sci 2007;22:173-6.8. Keane JR. ird nerve palsy: Analysis of 1400 personally-examined inpatients. Can J Neurol Sci 2010;37:662-70.9. Laun A, Tonn JC. Cranial nerve lesions following subarachnoid hemorrhage and aneurysm of the circle of willis. Neurosurg Rev 1988;11:137-41.10. Linskey ME, Sekhar LN, Hirsch W Jr., Yonas H, Horton JA. Aneurysms of the intracavernous carotid artery: Clinical presentation, radiographic features, and pathogenesis. Neurosurgery 1990;26:71-9.11. Nieuwkamp DJ, Setz LE, Algra A, Linn FH, de Rooij NK, Rinkel GJ, et al. Changes in case fatality of aneurysmal subarachnoid haemorrhage over time, according to age, sex, and region: A meta-analysis. Lancet Neurol 2009;8:635-42.12. Park HK, Rha HK, Lee KJ, Chough CK, Joo W. Microsurgical anatomy of the oculomotor nerve. Clin Anat 2017;30:21-31.13. Plum F, Posner JB. In: Davis F, editor. e Diagnosis of Stupor and Coma. 3rd ed. Philadelphia, PA: F. A. Davis Co.; 1980.14. Shukla DP, Bhat DI, Devi BI. Anterior communicating artery aneurysm presenting with vision loss. J Neurosci Rural Pract 2013;4:305-7.15. Somagawa C, Fukuda Y, Yoshimura S, Satoh K, Hiu T, Ono T, et al. A rare case of ruptured internal carotid-posterior communicating artery aneurysm associated with contralateral delayed oculomotor nerve palsy. No Shinkei Geka 2017;45:629-35.Finger, et al.: Contralateral oculomotor nerve palsy by ruptured aneurysm in the posterior communicating segment of carotid arterySurgical Neurology International • 2019 • 10(177) | 516. Soni SR. Aneurysms of the posterior communicating artery and oculomotor paresis. J Neurol Neurosurg Psychiatry 1974; 37:475-84.17. Sun Y, Li G, Hou K, Gao X, Zhu X. A  case of delayed contralateral oculomotor nerve palsy after microsurgical clipping of a posterior communicating artery aneurysm. Int J Clin Exp Med 2016;9:12964-6.18. van Gijn J, Kerr RS, Rinkel GJ. Subarachnoid haemorrhage. Lancet 2007;369:306-18.How to cite this article: Finger G, Martins OG, Nesi WM, Casarin MC, de Almeida LP, Schiavo FL, et al. Ruptured aneurysm in the posterior communicating segment of carotid artery presenting with contralateral oculomotor nerve palsy. Surg Neurol Int 2019;10:177.19. Yanaka K, Matsumaru Y, Mashiko R, Hyodo A, Sugimoto K, Nose T, et al. Small unruptured cerebral aneurysms presenting with oculomotor nerve palsy. Neurosurgery 2003;52:553-7.

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Ruptured aneurysm in the posterior communicating segment of carotid artery presenting with contralateral oculomotor nerve palsy

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