Progesterone for acute traumatic brain injury

Systematic reviews

2016

Ma et al., updated the searches of the following databases: the Cochrane Injuries Group’s Specialised Register (30 September 2016), the Cochrane Central Register of Controlled Trials (CENTRAL; Issue 9, 2016), MEDLINE (Ovid; 1950 to 30 September 2016), Embase (Ovid; 1980 to 30 September 2016), Web of Science Core Collection: Conference Proceedings Citation Index-Science (CPCI-S; 1990 to 30 September 2016); and trials registries: Clinicaltrials.gov (30 September 2016) and the World Health Organization (WHO) International Clinical Trials Registry Platform (30 September 2016).
They included randomised controlled trials (RCTs) of progesterone versus no progesterone (or placebo) for the treatment of people with acute TBI.
Two review authors screened search results independently to identify potentially relevant studies for inclusion. Independently, two review authors selected trials that met the inclusion criteria from the results of the screened searches, with no disagreement.
They included five RCTs in the review, with a total of 2392 participants. We assessed one trial to be at low risk of bias; two at unclear risk of bias (in one multicentred trial the possibility of centre effects was unclear, whilst the other trial was stopped early), and two at high risk of bias, due to issues with blinding and selective reporting of outcome data.All included studies reported the effects of progesterone on mortality and disability. Low quality evidence revealed no evidence of a difference in overall mortality between the progesterone group and placebo group (RR 0.91, 95% CI 0.65 to 1.28, I² = 62%; 5 studies, 2392 participants, 2376 pooled for analysis). Using the GRADE criteria, we assessed the quality of the evidence as low, due to the substantial inconsistency across studies.There was also no evidence of a difference in disability (unfavourable outcomes as assessed by the Glasgow Outcome Score) between the progesterone group and placebo group (RR 0.98, 95% CI 0.89 to 1.06, I² = 37%; 4 studies; 2336 participants, 2260 pooled for analysis). We assessed the quality of this evidence to be moderate, due to inconsistency across studies.Data were not available for meta-analysis for the outcomes of mean intracranial pressure, blood pressure, body temperature or adverse events. However, data from three studies showed no difference in mean intracranial pressure between the groups. Data from another study showed no evidence of a difference in blood pressure or body temperature between the progesterone and placebo groups, although there was evidence that intravenous progesterone infusion increased the frequency of phlebitis (882 participants). There was no evidence of a difference in the rate of other adverse events between progesterone treatment and placebo in the other three studies that reported on adverse events.
This updated review did not find evidence that progesterone could reduce mortality or disability in patients with TBI. However, concerns regarding inconsistency (heterogeneity among participants and the intervention used) across included studies reduce our confidence in these results.There is no evidence from the available data that progesterone therapy results in more adverse events than placebo, aside from evidence from a single study of an increase in phlebitis (in the case of intravascular progesterone).There were not enough data on the effects of progesterone therapy for our other outcomes of interest (intracranial pressure, blood pressure, body temperature) for us to be able to draw firm conclusions.Future trials would benefit from a more precise classification of TBI and attempts to optimise progesterone dosage and scheduling 1).

2012

Ma et al., searched: the Cochrane Injuries Group’s Specialised Register (13 July 2012), Cochrane Central Register of Controlled Trials (CENTRAL) (Issue 7, 2012), MEDLINE (Ovid) (1950 to August week 1, 2012), EMBASE (Ovid) (1980 to week 32 2012), LILACS (12 August 2012), Zetoc (13 July 2012), Clinicaltrials.gov (12 August 2012), Controlled-trials.com (12 August 2012). SELECTION CRITERIA: We included published and unpublished randomised controlled trials (RCTs) of progesterone versus no progesterone (or placebo) for the treatment of people with acute TBI. DATA COLLECTION AND ANALYSIS: Two review authors independently screened search results to identify the full texts of potentially relevant studies for inclusion. From the results of the screened searches two review authors independently selected trials meeting the inclusion criteria, with no disagreement. MAIN RESULTS: Three studies were included with a total of 315 people. Two included studies were of high methodological quality, with low risk of bias in allocation concealment, blinding and incomplete outcome data. One study did not use blinding and had unclear risk of bias in allocation concealment and incomplete outcome data. All three studies reported the effects of progesterone on mortality. The pooled risk ratio (RR) for mortality at end of follow-up was 0.61, 95% confidence interval (CI) 0.40 to 0.93. Three studies measured disability and found the RR of death or severe disability in patients treated with progesterone to be 0.77, 95% CI 0.62 to 0.96. Data from two studies showed no difference in mean intracranial pressure or the rate of adverse and serious adverse events among people in either group. One study presented blood pressure and temperature data, and there were no differences between the people in the progesterone or control groups. There was no substantial evidence for the presence of heterogeneity.
Current clinical evidence from three small RCTs indicates progesterone may improve the neurologic outcome of patients suffering TBI. This evidence is still insufficient and further multicentre randomised controlled trials are required 2).

2011

Junpeng et al., searched: the Cochrane Injuries Group’s Specialised Register (to April 2010), Cochrane Central Register of Controlled Trials 2010, Issue 1 (The Cochrane Library), MEDLINE (Ovid) (1950 to April week 1 2010), EMBASE (Ovid) (1980 to week 14 2010), LILACS (to 17 April 2010 ), Zetoc (to 21 April 2010), Clinicaltrials.gov (17 April 2010 ), Controlled-trials.com (17 April 2010).
They included published and unpublished randomised controlled trials (RCTs) of progesterone versus no progesterone (or placebo) for the treatment of acute TBI.
Two authors independently screened search results to identify the full texts of potentially relevant studies for inclusion. From the results of the screened searches two authors independently selected trials meeting the inclusion criteria, with no disagreement.
Three studies were included with 315 patients. All three studies reported the effects of progesterone on mortality. The pooled relative risk (RR) for mortality at end of follow-up is 0.61, 95% confidence interval (CI) 0.40 to 0.93. Three studies measured disability and found the RR of death or severe disability in patients treated with progesterone was 0.77, 95% confidence interval (CI) 0.62 to 0.96. Two studies presented data on intracranial pressure and adverse events. One study presented blood pressure and temperature data. There was no substantial evidence for the presence of heterogeneity.
Current clinical evidence from three small RCTs indicates progesterone may improve the neurologic outcome of patients suffering TBI. This evidence is still insufficient and further multicentre randomised controlled trials are required 3).


Progesterone has been associated with robust positive effects in animal models of traumatic brain injury (TBI) and with clinical benefits in two phase 2 randomized controlled trials. Skolnick et al, investigated the efficacy and safety of progesterone in a large, prospective, phase 3 randomized controlled trial.
A multinational placebo controlled study, in which 1195 patients, 16 to 70 years of age, with severe traumatic brain injury TBI (Glasgow Coma Scale score, ≤8 (on a scale of 3 to 15, with lower scores indicating a reduced level of consciousness and at least one reactive pupil) were randomly assigned to receive progesterone or placebo. Dosing began within 8 hours after injury and continued for 120 hours. The primary efficacy end point was the Glasgow Outcome Scale score at 6 months after the injury.
Proportional-odds analysis with covariate adjustment showed no treatment effect of progesterone as compared with placebo (odds ratio, 0.96; confidence interval, 0.77 to 1.18). The proportion of patients with a favorable outcome on the Glasgow Outcome Scale (good recovery or moderate disability) was 50.4% with progesterone, as compared with 50.5% with placebo. Mortality was similar in the two groups. No relevant safety differences were noted between progesterone and placebo.
Primary and secondary efficacy analyses showed no clinical benefit of progesterone in patients with severe TBI. These data stand in contrast to the robust preclinical data and results of early single-center trials that provided the impetus to initiate phase 3 trials. (Funded by BHR Pharma; SYNAPSE ClinicalTrials.gov number, NCT01143064 .) 4).
There was no significant difference between the progesterone group and the placebo group in the proportion of patients with a favorable outcome (relative benefit of progesterone, 0.95; 95% confidence interval [CI], 0.85 to 1.06; P=0.35). Phlebitis or thrombophlebitis was more frequent in the progesterone group than in the placebo group (relative risk, 3.03; CI, 1.96 to 4.66). There were no significant differences in the other prespecified safety outcomes. Conclusions This clinical trial did not show a benefit of progesterone over placebo in the improvement of outcomes in patients with acute TBI. (Funded by the National Institute of Neurological Disorders and Stroke and others; PROTECT III ClinicalTrials.gov number, NCT00822900 .) 5).


There is significant theoretical evidence for the potential role of estrogen and progesterone use in altering the pathogenesis of SAH. Nevertheless, this has received mixed reviews in both case controlled studies and cohort analysis within the literature 6)

1) Ma J, Huang S, Qin S, You C, Zeng Y. Progesterone for acute traumatic brain injury. Cochrane Database Syst Rev. 2016 Dec 22;12:CD008409. doi: 10.1002/14651858.CD008409.pub4. [Epub ahead of print] Review. PubMed PMID: 28005271.
2) Ma J, Huang S, Qin S, You C. Progesterone for acute traumatic brain injury. Cochrane Database Syst Rev. 2012 Oct 17;10:CD008409. doi: 10.1002/14651858.CD008409.pub3. Review. PubMed PMID: 23076947.
3) Junpeng M, Huang S, Qin S. Progesterone for acute traumatic brain injury. Cochrane Database Syst Rev. 2011 Jan 19;(1):CD008409. doi: 10.1002/14651858.CD008409.pub2. Review. Update in: Cochrane Database Syst Rev. 2012;10:CD008409. PubMed PMID: 21249708.
4) Skolnick BE, Maas AI, Narayan RK, van der Hoop RG, MacAllister T, Ward JD, Nelson NR, Stocchetti N; the SYNAPSE Trial Investigators. A Clinical Trial of Progesterone for Severe Traumatic Brain Injury. N Engl J Med. 2014 Dec 10. [Epub ahead of print] PubMed PMID: 25493978.
5) Wright DW, Yeatts SD, Silbergleit R, Palesch YY, Hertzberg VS, Frankel M, Goldstein FC, Caveney AF, Howlett-Smith H, Bengelink EM, Manley GT, Merck LH, Janis LS, Barsan WG; the NETT Investigators. Very Early Administration of Progesterone for Acute Traumatic Brain Injury. N Engl J Med. 2014 Dec 10. [Epub ahead of print] PubMed PMID: 25493974.
6) Young AM, Karri SK, Ogilvy CS. Exploring the use of estrogen & progesterone replacement therapy in subarachnoid hemorrhage. Curr Drug Saf. 2012 Jul;7(3):202-6. Review. PubMed PMID: 22950381.

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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.
2) Kassis SZ, Jouanneau E, Tahon FB, Salkine F, Perrin G, Turjman F. Recovery of third nerve palsy after endovascular treatment of posterior communicating artery aneurysms. World Neurosurg. 2010;73:11–6.
3) Hamer J. Prognosis of oculomotor palsy in patients with aneurysms of the posterior communicating artery. Acta Neurochir (Wien). 1982;66(3-4):173-85. PubMed PMID: 7168392.
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.
5) Gaberel T, Borha A, Palma CD, Emery E. Clipping versus coiling in the management of posterior communicating artery aneurysms with third nerve palsy: a systematic review and meta-analysis. World Neurosurg. 2015 Sep 23. pii: S1878-8750(15)01189-4. doi: 10.1016/j.wneu.2015.09.026. [Epub ahead of print] PubMed PMID: 26409080.
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.
8) Zheng F, Dong Y, Xia P, Mpotsaris A, Stavrinou P, Brinker G, Goldbrunner R, Krischek B. 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. Clin Neurol Neurosurg. 2016 Dec 11;153:20-26. doi: 10.1016/j.clineuro.2016.11.022. [Epub ahead of print] Review. PubMed PMID: 28006728.
9) Lv N, Yu Y, Xu J, Karmonik C, Liu J, Huang Q. Hemodynamic and morphological characteristics of unruptured posterior communicating artery aneurysms with oculomotor nerve palsy. J Neurosurg. 2015 Dec 4:1-5. [Epub ahead of print] PubMed PMID: 26636379.
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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