Oculomotor nerve palsy in chronic subdural hematoma

Oculomotor nerve palsy in chronic subdural hematoma

Isolated oculomotor nerve palsy is well known as a symptom of microvascular infarction and intracranial aneurysm, but unilateral oculomotor nerve palsy as an initial manifestation of chronic subdural hematoma (CSDH) is a rare clinical condition.

Oculomotor nerve palsy (ONP) usually occurs in chronic subdural hematoma (CSDH) as a common sign of brain herniation that typically is associated with a deterioration of consciousness.


Ninety-eight cases of cSDH were operated over a 6-year period, in which 14 cases were classified as being bilateral. Among these 14 cases, 6 cases showed a rapid and aggressive clinical course. Therefore, complicated risk factors, the initial data on coagulofibrinolytic examination, magnetic resonance imaging appearance, and prognosis were analyzed.

Of the 6 cases, 5 showed a rapid aggravation as they awaited surgery. The period of the aggravation since the initial diagnosis harboring cSDH was 19 to 54 hours. One case was at first neurologically free from any disturbance but 17 hours later experienced a generalized seizure. All 6 cases experienced consciousness disturbance. In addition, 3 of them manifested oculomotor palsy 1).

Case reports

Zavatto et al., reported a bilateral oculomotor palsy after surgical evacuation of chronic subdural hematoma 2).


Corrivetti et al., reported 2 cases of bilateral CSDH who presented with ONP without deterioration of consciousness. An extensive literature reviewrevealed this is an extremely rare finding.

They also investigated all the possible pathogenic mechanisms producing nerve impairment and found a strong association with bilateral subdural hematoma. Vascular compression between posterior circulation arteries and tentorial edge abnormalities also could be involved. Vulnerability of the oculomotor nerve seems to be a necessary condition leading to clinical onset and is caused by predisposing factors to nerve damage, including vascular disease, head trauma, or herpes zoster infection.

Although isolated ONP is a very rare presentation of CSDH, a differential diagnosis is absolutely necessary, because surgical treatment allows good recovery of third nerve palsy in most of the cases 3).


Matsuda et al., reported a rare case of an 84-year-old woman with bilateral CSDH who presented with unilateral oculomotor nerve palsy as the initial symptom. The patient, who had a medical history of minor head injury 3 weeks prior, presented with left ptosis, diplopia, and vomiting. She had taken an antiplatelet drug for lacunar cerebral infarction. Computed tomography (CT) of the head showed bilateral CSDH with a slight midline shift to the left side. She underwent an urgent evacuation through bilateral frontal burr holes. Magnetic resonance angiography (MRA) after evacuation revealed no intracranial aneurysms, but constructive interference in steady-state (CISS) magnetic resonance imaging (MRI) revealed that the left posterior cerebral artery (PCA) ran much more anteriorly and inferiorly compared with the right PCA and the left oculomotor nerve passed very closely between the left PCA and the left superior cerebellar artery (SCA). There is the possibility that the strong compression to the left uncus, the left PCA, and the left SCA due to the bilateral CSDH resulted in left oculomotor nerve palsy with an initial manifestation without unconsciousness. Unilateral oculomotor nerve palsy as an initial presentation caused by bilateral CSDH without unconsciousness is a rare clinical condition, but this situation is very important as a differential diagnosis of unilateral oculomotor nerve palsy 4).


Jalil et al., reported the case of a patient who presented with left oculomotor cranial nerve palsy with an associated large volume left acute on chronic subdural haematoma. Coincidentally, this woman was also found to have a recent history of herpes zoster ophthalmicus 5).


Moon et al., reported two cases of Kernohan’s notch phenomenon secondary to chronic subdural hematoma detected by MRI. In the first case, the patient was drowsy with an oculomotor palsy and a hemiparesis ipsilateral to the chronic subdural hematoma. MRI in the post-operative period showed no abnormal signal or deformity of the crus cerebri. The neurological signs immediately resolved after trephination. In the second case, the patient was admitted with progressive decrease in their level of consciousness and ipsilateral hemiparesis with the chronic subdural hematoma. MRI on admission revealed an abnormal signal in the contralateral crus cerebri against the chronic subdural hematoma. After surgery, the mental state gradually recovered to normal with some degree of residual hemiparesis. In patients with chronic subdural hematoma, a compressive deformity of the crus cerebri, without abnormal signal on MRI, may predict a better neurological recovery in patients with Kernohan’s notch phenomenon 6).


Mishra et al., reported a 50-year old male patient with complaints of drooping of the right upper eyelid, for the past 1 day. He also gave a history of generalized mild headache for the past 1 week. There was no history of any injury, vomiting, fever, seizures, loss of consciousness, slurred speech, numbness, weakness, diplopia or any other major systemic illnesses like hypertension or diabetes. The patient also gave no history of any cardiovascular disorder. Patient was not a known alcoholic and neither was he on any anti coagulant or anti platelet therapy. On examination the patient was conscious and well oriented in time and space. His vitals were all within normal limits. Neurological examination was strictly unremarkable. Blood test revealed a normal blood count, urea, creatinine and electrolytes and was also negative for HIV antibodies. Ocular examination of the right eye revealed a vision of 6/9, improving to 6/6 with pin hole. There was severe ptosis with the marginal reflex distance 1 (MRD1) < −0.5 mm and a poor levator function (<4 mm). The eyeball too was displaced outwards and downwards (infraducted and abducted). The ocular movements were severely affected, with an absence of adduction and elevation; however abduction was full with mild residual depression. Depression was accompanied by intorsion, maximally when the eye was abducted. The pupil was dilated (6 mm) and un-reactive to light (vs. 3 mm and reactive in the left eye). Fundus was essentially normal. The left eye was uninvolved. A provisional diagnosis of isolated unilateral oculomotor nerve palsy, right eye, was made and the suspected site of involvement of the nerve was clinically deduced to be around the fascicular subarachnoid portion. This is because the fascicles of the third cranial nerve exit the mid brain through the medial aspect of the cerebral peduncles and are not near any other cranial nerves at this point. So isolated third cranial nerve palsy occurs from lesions in this location. Aneurysm is the most common lesion to affect the third cranial nerve in the subarachnoid space. The fact that the pupil too was involved pointed towards a posterior communicating artery aneurysm. A provisional diagnosis of a posterior communicating artery aneurysm with or without overt subarachnoid haemorrhage was made and the patient was sent for an urgent computed tomography (CT scan) of the brain and orbits, which revealed a CSDH in the right fronto-temporo-parietal lobe, causing mass effect in the form of compression of the right lateral ventricle and a midline shift of 16.5 mm. The patient was immediately transferred to a higher neurological centre where he underwent evacuation of the haematoma via a right frontal burr hole surgery. Post operative period was uneventful and the patient was put on anti epileptics (tablet dilantin 300 mg once daily), observed for 2 months and then sent on 04 weeks sick leave. His oculomotor nerve palsy gradually recovered completely and CT scan brain repeated on his return from sick leave showed a complete resolution of the haematoma. He was finally discharged back to his unit with no residual adverse effects whatsoever 7).


Cortes-Franco et al.,published in 2006 a Isolated IIIrd nerve palsy as the only sign of chronic subdural haematoma 8).


Ortega-Martínez et al., reported a patient with a chronic subdural hematoma that presented with a complete third nerve palsy and normal consciousness. Complete recovery was achieved after surgical evacuation. Rebleeding within the hematoma cavity, most possibly favored by antiaggregating agents, was considered responsible for this rare presentation. In these cases expeditious surgical evacuation is indicated 9).


A case of a 41-year-old man with a 1-month history of postural headache due to spontaneous intracranial hypotension (SIH). His MRI revealed bilateral chronic subdural hematoma (CSH) and diffuse dural enhancement after gadolinium infusion. Indium-111 radionuclide cisternography revealed a CSF leak from the cervico-thoracic junction and rapid accumulation of radioisotope in the bladder. Postural headache failed to resolve with prolonged bed rest. The patient became restless and suffered recent memory disturbance. We therefore decided to treat the CSF leak with an epidural blood patch. After the procedure, the patient’s headache resolved completely. However one day later, left oculomotor nerve palsy developed. MRI revealed enlargement of the left CSH with mass effect and midline shift. After hematoma drainage, the patient became alert and oculomotor palsy recovered gradually. To treat cases of CSH with SIH, the best method is to repair the CSF leakage and treat subdural hematoma at the same time. If the patient shows depressed consciousness, we recommend initial drainage of the subdural hematoma, because, following the repair of CSF leakage, mass effect such as uncal herniation may occur 10).


An 85-year-old male presented with bilateral chronic subdural hematomas (CSDHs) resulting in unilateral oculomotor nerve paresis and brainstem symptoms immediately after removal of both hematomas in a single operation. Initial computed tomography on admission demonstrated marked thick bilateral hematomas buckling the brain parenchyma with a minimal midline shift. Almost simultaneous removal of the hematomas was performed with the left side was decompressed first with a time difference of at most 2 minutes. However, the patient developed right oculomotor nerve paresis, left hemiparesis, and consciousness disturbance after the operation. The relatively marked increase in pressure on the right side may have caused transient unilateral brain stem compression and herniation of unilateral medial temporal lobe during the short time between the right and left procedures. Another factor was the vulnerability of the oculomotor nerve resulting from posterior replacement of the brain stem and stretching of the oculomotor nerves as seen on sagittal magnetic resonance (MR) images. Axial MR images obtained at the same time demonstrated medial deflection of the distal oculomotor nerve after crossing the posterior cerebral artery, which indicates previous transient compression of the nerve and the brain stem. Gradual and symmetrical decompression without time lag is recommended for the treatment of huge bilateral CSDHs 11).


In 1994 Phookan and Cameron published a bilateral chronic subdural haematoma with isolated oculomotor nerve palsy 12).


Crone et al published in 1985 a patient with adult-onset diabetes mellitus who developed an oculomotor palsy with pupillary sparing. Five days after her initial evaluation, she presented in a confused state with a complete oculomotor palsy. Computed cranial tomography revealed a chronic subdural hematoma. They recommend that noninvasive radiographic intracranial investigation be considered in elderly patients with adult-onset diabetes mellitus who present with headache and pupil-sparing oculomotor palsy 13).

References

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Kurokawa Y, Ishizaki E, Inaba K. Bilateral chronic subdural hematoma cases showing rapid and progressive aggravation. Surg Neurol. 2005 Nov;64(5):444-9; discussion 449. PubMed PMID: 16253697.
2)

Zavatto L, Marrone F, Allevi M, Ricci A, Taddei G. Bilateral oculomotor palsy after surgical evacuation of chronic subdural hematoma. World Neurosurg. 2019 Apr 10. pii: S1878-8750(19)31035-6. doi: 10.1016/j.wneu.2019.04.043. [Epub ahead of print] PubMed PMID: 30980981.
3)

Corrivetti F, Moschettoni L, Lunardi P. Isolated Oculomotor Nerve Palsy as Presenting Symptom of Bilateral Chronic Subdural Hematomas: Two Consecutive Case Report and Review of the Literature. World Neurosurg. 2016 Apr;88:686.e9-12. doi: 10.1016/j.wneu.2015.11.012. Epub 2015 Nov 14. Review. PubMed PMID: 26585722.
4)

Matsuda R, Hironaka Y, Kawai H, Park YS, Taoka T, Nakase H. Unilateral oculomotor nerve palsy as an initial presentation of bilateral chronic subdural hematoma: case report. Neurol Med Chir (Tokyo). 2013;53(9):616-9. PubMed PMID: 24067774; PubMed Central PMCID: PMC4508681.
5)

Jalil MF, Tee JW, Han T. Isolated III cranial nerve palsy: a surprising presentation of an acute on chronic subdural haematoma. BMJ Case Rep. 2013 Jun 19;2013. pii: bcr2013009992. doi: 10.1136/bcr-2013-009992. PubMed PMID: 23784767; PubMed Central PMCID: PMC3702887.
6)

Moon KS, Lee JK, Joo SP, Kim TS, Jung S, Kim JH, Kim SH, Kang SS. Kernohan’s notch phenomenon in chronic subdural hematoma: MRI findings. J Clin Neurosci. 2007 Oct;14(10):989-92. PubMed PMID: 17823049.
7)

Mishra A, Shukla S, Baranwal VK, Patra VK, Chaudhary B. Isolated unilateral IIIrd nerve palsy as the only sign of chronic subdural haematoma. Med J Armed Forces India. 2015 Jul;71(Suppl 1):S127-30. doi: 10.1016/j.mjafi.2013.07.009. Epub 2013 Sep 26. PubMed PMID: 26265807; PubMed Central PMCID: PMC4529560.
8)

Cortes-Franco S, García-Marín VM, Pacheco-Abreu EM, Roldán Delgado H. [Isolated IIIrd nerve palsy as the only sign of chronic subdural haematoma]. Med Clin (Barc). 2006 Sep 30;127(12):479. Spanish. PubMed PMID: 17040640.
9)

Ortega-Martínez M, Fernández-Portales I, Cabezudo JM, Rodríguez-Sánchez JA, Gómez-Perals LF, Giménez-Pando J. [Isolated oculomotor palsy. An unusual presentation of chronic subural hematoma]. Neurocirugia (Astur). 2003 Oct;14(5):423-5; discussion 425. Spanish. PubMed PMID: 14603390.
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Mikawa S, Ebina T. [Spontaneous intracranial hypotension complicating subdural hematoma: unilateral oculomotor nerve palsy caused by epidural blood patch]. No Shinkei Geka. 2001 Aug;29(8):747-53. Review. Japanese. PubMed PMID: 11554093.
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Okuchi K, Fujioka M, Maeda Y, Kagoshima T, Sakaki T. Bilateral chronic subdural hematomas resulting in unilateral oculomotor nerve paresis and brain stem symptoms after operation–case report. Neurol Med Chir (Tokyo). 1999 May;39(5):367-71. PubMed PMID: 10481440.
12)

Phookan G, Cameron M. Bilateral chronic subdural haematoma: an unusual presentation with isolated oculomotor nerve palsy. J Neurol Neurosurg Psychiatry. 1994 Sep;57(9):1146. PubMed PMID: 8089699; PubMed Central PMCID: PMC1073157.
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Crone KR, Lee KS, Davis CH Jr. Oculomotor palsy with pupillary sparing in a patient with chronic subdural hematoma. Surg Neurol. 1985 Dec;24(6):668-70. PubMed PMID: 4060048.

Is clipping better than coiling in the treatment of patients with oculomotor nerve palsies induced by posterior communicating artery aneurysms? A systematic review and meta-analysis

Oculomotor nerve palsy (ONP) is often the presenting symptom in patients with posterior communicating artery aneurysms with variable recovery of oculomotor nerve function following treatment.
Unruptured posterior communicating artery (PCoA) aneurysms with oculomotor nerve palsy (ONP) have a very high risk of rupture.
ONP can occur with PCOMM aneurysm with or without subarachnoid hemorrhage (SAH) 1).

Epidemiology

It has been estimated that oculomotor nerve palsy (OMNP) occurs in up to one-third of patients with posterior communicating artery aneurysms due to a mass effect on the oculomotor nerve 2).

Outcome

The prognosis of oculomotor palsy mainly depends on the interval between the onset of palsy and the time of operation, and furthermore on the degree of preoperative deficit and the development of the cranial nerve lesion. The incidence of ultimately complete or incomplete palsy is the same in cases with subarachnoid haemorrhage and without rupture (“warning symptom”).
In many cases, an initially incomplete paresis develops to a complete ocular palsy within eight days. Ptosis is generally the first symptom, and it frequently shows the earliest recovery of all other disturbed oculomotor functions after surgery. Full recovery of oculomotor palsy occurs usually only in those patients who undergo early clipping of an aneurysm, i.e. mainly within 10 days after onset of ocular palsy. Complete restitution after carotid ligation is possible, but rare. In cases with full recovery, restitution occurs mostly within three months, sometimes even within a few weeks. An improvement in oculomotor palsy is still possible after a year, but ultimately in these patients recovery remains always more or less incomplete. Incomplete restitution of a third cranial nerve lesion is very often associated with aberrant regeneration and subsequent synkinetic ocular movement. The restitution of the single ocular muscle functions shows a fairly constant course: the levator palpebrae muscle and the M. rectus medialis show rapid recovery. The parasympathetic fibres follow next, but normal function of elevation and depression of the ocular bulb (M. rectus sup., M. obliquus inf. and M. rectus inf.) is often delayed 3).
Patients with ONP secondary to PCoA aneurysms treated with clipping showed higher rates of full ONP resolution than patients treated with coil embolization. Larger prospective studies are needed to determine the true potential of recovery associated with each treatment 4).
Eleven relevant studies involving a total of 384 patients with third nerve palsy due to PCoA aneurysms at baseline, of whom 257 (67.0%) were treated by clipping and 127 by coiling (33.0%), were included in a meta-analysis. Pooled Odds Ratios of the impact of clipping or coiling on complete ONP recovery, lack of ONP recovery and procedure-related death were calculated. The overall complete ONP recovery rate was 42.5% in the coiling group compared to 83.6% in the clipping group. The increase in complete ONP recovery in the clipping group corresponds to an overall pooled Mantel-Haenzel odds ratio of 4.44 (95% CI 1.66-11.84). Subgroup analysis revealed a clear benefit of clipping over coiling in patients with ruptured aneurysms, but not in unruptured aneurysms. None of the eleven studies reported any procedure-related death.
Surgical clipping of PCoA aneurysms causing third nerve palsy achieves better ONP recovery than endovascular coiling. This result could be particularly true in the case of ruptured aneurysms. In view of the purely observational data, statements about this effect should be made with great caution. A randomized trial would address the therapeutic dilemma involved better, but pending the results of such a trial, we recommend treating PCoA artery aneurysms causing ONP with surgery 5).
Simultaneous elimination of 2 injury mechanisms, compression and pulsation, when treating the oculomotor nerve by surgical clipping may be more advantageous than endovascular embolization 6).

Mecobalamin treatment

27 patients were given embolization treatment and 28 received embolization + mecobalamin treatment. The recovery condition of ONP were followed and compared one year after the treatment.
All patients were followed up for more than a year. And 31 patients (56.4%) out of 55 achieved complete recovery, 19 (34.5%) attained partial recovery and 5 (9.1%) had no recovery from ONP. Whereas, 20 patients (71.4%) in the embolization + mecobalamin treatment group achieved complete recovery and 11 (40.7%) in the embolization treatment group achieved partial recovery, and the comparative difference was statistically significant (p < 0.05).
Endovascular is highly efficacious treatment for ONP-inducing PcomA and can promote the recovery of oculomotor nerve palsy after embolism 7).

Systematic reviews

A meta-analysis of studies that compared surgical clipping with endovascular coiling was conducted by searching the literature via Pubmed, Embase and Cochrane Library databases without restricting the publication year. We extracted the following information: author names and publication year; clinical outcome (number of complete and incomplete recovery of ONP); perioperative data (number of pre-operatively complete or incomplete ONP, subarachnoid hemorrhage or not, number of complications (hydrocephalus, recurrence of PcomAA)). Except for author names and publication year, the data was pooled to perform a mean effect size estimate. The effects of two treatment modalities were then analyzed.
Nine published reports of eligible studies involving 297 participants met the inclusion criteria. Overall, compared with endovascular coiling, surgical clipping had no statistically significant difference on the complete recovery of ONP, although there was an obvious trend in favor of clipping [RR=1.48, 95%CI (0.95, 2.29), p=0.08]. There was no significant difference in the total efficiency (any degree of change) on ONP [RR=1.08, 95%CI (0.94, 1.25), p>0.05], the overall complications [RR=0.60, 95%CI (0.33, 1.10), p>0.05], the efficacy on the complete recovery of ONP in patients without SAH [RR=0.83, 95%CI (0.53, 1.31), p>0.05], the effect on the complete recovery of ONP in patients with pre-operatively complete or incomplete ONP [RR=1.12, 95%CI (0.68, 1.85), p>0.05], [RR=1.12, 95%CI (0.79, 1.59), p>0.05]. In a comparison of a small cohort of patients that had suffered an SAH (17 vs. 22) there was a significant difference on the effect on complete recovery of ONP between clipping and coiling [RR=1.70, 95%CI (1.08, 2.67), p<0.05].
A superiority of clipping over coiling for the complete recovery of oculomotor nerve palsy in patients that had suffered an SAH from a ruptured aneurysm of the posterior communicating artery was found in the present meta-analysis. Limited by the relatively small sample sizes included, there were no significant differences observed in the clinical outcome between coiling and clipping in the treatment of unruptured PcomAA causing ONP. More evidence from advanced multi-center studies of large scale is needed to provide insight into the optimal treatment for outcome of ONP caused by PcomAAs 8).

Case series

2016

Fourteen unruptured PCoA aneurysms with ONP, 33 ruptured PCoA aneurysms, and 21 asymptomatic unruptured PCoA aneurysms were included in a study. The clinical, morphological, and hemodynamic characteristics were compared among the different groups.
The clinical characteristics did not differ among the 3 groups (p > 0.05), whereas the morphological and hemodynamic analyses showed that size, aspect ratio, size ratio, undulation index, nonsphericity index, ellipticity index, normalized wall shear stress (WSS), and percentage of low WSS area differed significantly (p < 0.05) among the 3 groups. Furthermore, multiple comparisons revealed that these parameters differed significantly between the ONP group and the asymptomatic unruptured group and between the ruptured group and the asymptomatic unruptured group, except for size, which differed significantly only between the ONP group and the asymptomatic unruptured group (p = 0.0005). No morphological or hemodynamic parameters differed between the ONP group and the ruptured group.
Unruptured PCoA aneurysms with ONP demonstrated a distinctive morphological-hemodynamic pattern that was significantly different compared with asymptomatic unruptured PCoA aneurysms and was similar to ruptured PCoA aneurysms. The larger size, more irregular shape, and lower WSS might be related to the high rupture risk of PCoA aneurysms 9).

2015

230 PCOMM aneurysm endovascular coilings between the years 2006 and 2011, of which 20 cases presented with ONP. Sheehan et al. recorded the degree of nerve recovery – complete, partial or none – while also documenting other predictive factors, such as degree of pre-intervention nerve deficit, presence of subarachnoid haemorrhage (SAH), size and location of the PCOMM aneurysm and length of follow-up.
Of the 20 patients, 9 (45%) presented with complete ONP and 11 (55%) with partial ONP. After an average follow-up period of 16 months, all patients achieved oculomotor nerve recovery; 9 (45%) patients had complete recovery and 11 (55%) patients had partial recovery. Of the 9 patients who presented with complete ONP, 5 (56%) patients made a complete recovery and 4 (44%) made a partial recovery. Of the 11 patients who initially presented with partial ONP, 4 (36%) made a complete recovery and 7 (64%) made a partial recovery. 7 (35%) patients also had a SAH, of whom 3 (43%) made a complete recovery with 4 (57%) making a partial recovery10).

1974

One hundred and seventy-four patients with a posterior communicating aneurysm were seen over a 21 year period. There was a ratio of four females to one male and women were on average five years older. Fifty-nine (34%) had an oculomotor paresis. This group had up to four attacks of localized headache, large multiloculated aneurysms, and a greater time lapse from the onset of symptoms to surgery compared with those patients without oculomotor palsy. Delay in treatment allowed further attacks to occur which increased the mortality rate and decreased the chance that the eye would recover. Eighteen people who had had a palsy before craniotomy two to 18 years previously were examined. In four (22%) the paralysis had recovered completely, 14 (78%) had greatly reduced oculomotor function, and nine (50%) showed aberrant regeneration of the nerve. Nine of 62 patients, seven of whom were seen, developed a palsy after craniotomy and in five the eye had returned to normal 11).

1947

A paper is concerned with 55 aneurysms out of a total of 158 that caused isolated paralysis of the oculomotor nerve 12).

Case reports

2016

Binyamin et al report on two cases of resolution of third nerve palsy after flow diversion embolization of large and giant PCOM aneurysms without adjuvant coil placement. The resolution of third nerve palsy was not preceded by significant shrinkage of the aneurysmal sac on MRI. However, one patient showed resolution of T2-weighted signal abnormalities in the midbrain and mesial temporal lobe despite a similar size of the aneurysm. Therefore, flow diversion embolization of a PCOM aneurysm may resolve oculomotor nerve palsies through decreasing arterial pulsations against the nerve or midbrain 13).

1975

A patient had pupillary sparing the absence of subarachnoid bleeding. A few similar cases have appeared in the literature. The mechanism of pupillary sparing appears to be based on the position of the parasympathetic pupilloconstrictor fibers within the subarachnoid portion of the third nerve and on the anatomic relationship between the third nerve and the junction of the carotid and posterior communicating arteries 14).

1) Sheehan MJ, Dunne R, Thornton J, Brennan P, Looby S, O’Hare A. Endovascular repair of posterior communicating artery aneurysms, associated with oculomotor nerve palsy: A review of nerve recovery. Interv Neuroradiol. 2015 Jun;21(3):312-6. doi: 10.1177/1591019915583222. Epub 2015 May 26. PubMed PMID: 26015520.
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4) McCracken DJ, Lovasik BP, McCracken CE, Caplan JM, Turan N, Nogueira RG, Cawley CM, Dion JE, Tamargo RJ, Barrow DL, Pradilla G. Resolution of Oculomotor Nerve Palsy Secondary to Posterior Communicating Artery Aneurysms: Comparison of Clipping and Coiling. Neurosurgery. 2015 Aug 14. [Epub ahead of print] PubMed PMID: 26287555.
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6) Tan H, Huang G, Zhang T, Liu J, Li Z, Wang Z. A retrospective comparison of the influence of surgical clipping and endovascular embolization on recovery of oculomotor nerve palsy in patients with posterior communicating artery aneurysms. Neurosurgery. 2015 Jun;76(6):687-94; discussion 694. doi: 10.1227/NEU.0000000000000703. PubMed PMID: 25786201.
7) Wang SA, Yang J, Zhang GB, Feng YH, Wang F, Zhou PY. Effect of mecobalamin treatment on the recovery of patients with posterior communicating artery aneurysm inducing oculomotor nerve palsy after operation. Eur Rev Med Pharmacol Sci. 2015;19(14):2603-7. PubMed PMID: 26221889.
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10) Sheehan MJ, Dunne R, Thornton J, Brennan P, Looby S, O’Hare A. Endovascular repair of posterior communicating artery aneurysms, associated with oculomotor nerve palsy: A review of nerve recovery. Interv Neuroradiol. 2015 Jun;21(3):312-6. doi: 10.1177/1591019915583222. Epub 2015 May 26. PubMed PMID: 26015520.
11) Soni SR. Aneurysms of the posterior communicating artery and oculomotor paresis. J Neurol Neurosurg Psychiatry. 1974 Apr;37(4):475-84. PubMed PMID: 4838918; PubMed Central PMCID: PMC494681.
12) JEFFERSON G. Isolated oculomotor palsy caused by intracranial aneurysm. Proc R Soc Med. 1947 Jun;40(8):419-32. PubMed PMID: 20344031; PubMed Central PMCID: PMC2183530.
13) Binyamin TR, Dahlin BC, Waldau B. Resolution of third nerve palsy despite persistent aneurysmal mass effect after flow diversion embolization of posterior communicating artery aneurysms. J Clin Neurosci. 2016 May 12. pii: S0967-5868(16)30007-8. doi: 10.1016/j.jocn.2016.02.027. [Epub ahead of print] PubMed PMID: 27183957.
14) Kasoff I, Kelly DL Jr. Pupillary sparing in oculomotor palsy from internal carotid aneurysm. Case report. J Neurosurg. 1975 Jun;42(6):713-7. PubMed PMID: 1141967.
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