Posterior communicating artery aneurysm recurrence

Posterior communicating artery aneurysm recurrence

Seven of eight aneurysms (87.5%) were ruptured. Stent assisted coiling was used in one case that a stent was deployed via PCoA-ipsilateral P2 segment. The dual-microcatheter technique was used in one case. The remaining six cases were treated by coiling alone. One patient (12.5%) suffered perioperative complication, of which a coil herniated into parent vessel during the procedure without symptomatic stroke or other adverse event after the procedure. The initial embolization results showed complete occlusion in five cases and residual neck in three. Six patients (75%) had a mean of 15-month angiographic follow-up and two of them revealed recurrence (33.3%) 1)

Dome size, aneurysm neck width, aneurysm volume, and Pcom diameter were associated with recurrence after coil embolization for IC-PC ANs. In particular, Pcom diameter could be an independent risk factor for recurrence 2)).

Lee et al. from the Chuncheon Army Hospital and St. Mary’s Hospital in Seoul, demonstrated that fetal posterior cerebral artery may be an independent risk factor for the recurrence of posterior communicating artery aneurysms. Therefore, fetal-type posterior cerebral artery can be considered as an important risk factor for posterior communicating artery aneurysm recurrences, along with other known risk factors such as size, ruptured status, endovascular treatment, and incomplete occlusion 3).

In 2010 Golshani et al. from the Division of Vascular and Interventional Radiology, Duke University Medical CenterDurham published that coiled posterior communicating artery aneurysms have a particularly high risk of recurrence and must be followed closely. Posterior communicating artery aneurysms with an elongated fundus, true posterior communicating artery aneurysms, and aneurysms associated with a fetal posterior communicating artery may have better outcome with surgical clipping in terms of completeness of occlusion and preservation of the posterior communicating artery. However, as endovascular technology improves, endovascular treatment of posterior communicating artery aneurysms may become equivalent or preferable in the near future 4).


Liu J, Zhang Y, Li W, Wang K, Zhang Y, Yang X. Treatment of true posterior communicating artery aneurysms: Endovascular experience in a single center. Interv Neuroradiol. 2020 Feb;26(1):55-60. doi: 10.1177/1591019919874603. Epub 2019 Sep 5. PMID: 31488022; PMCID: PMC6998000.

Shinya Fukuta, Chiyoe Hikita, Mitsuhiro Iwasaki, Masahiro Maeda, Yasufumi Inaka, Hidekazu Yamazaki, Hiroaki Sato, Masafumi Morimoto, Hidenori Oishi, Risk factors for recurrence after coil embolization for internal carotid artery-posterior communicating artery aneurysms, Interdisciplinary Neurosurgery, Volume 24, 2021, 101097, ISSN 2214-7519, (

Lee HJ, Choi JH, Shin YS, Lee KS, Kim BS. Risk Factors for the Recurrence of Posterior Communicating Artery Aneurysm: The Significance of Fetal-Type Posterior Cerebral artery. J Stroke Cerebrovasc Dis. 2021 Apr 26;30(7):105821. doi: 10.1016/j.jstrokecerebrovasdis.2021.105821. Epub ahead of print. PMID: 33915389.

Golshani K, Ferrell A, Zomorodi A, Smith TP, Britz GW. A review of the management of posterior communicating artery aneurysms in the modern era. Surg Neurol Int 22-Dec-2010;1:88

Ocular toxocariasis

Ocular toxocariasis

see Toxocariasis.

see also Cerebral toxocariasis

Ocular toxocariasis (OT) is a zoonotic infection caused by larval stages of Toxocara canis and T. cati.

systematic review and meta-analysis aimed to evaluate the global prevalence of OT.

Five English (PubMedScopusScienceDirectWeb of Science, and Google Scholardatabases were explored and 101 articles met the inclusion criteria.

The pooled prevalence (95% confidence interval) of OT was higher in immunological studies (9%. 6-12%) than in studies that applied ophthalmic examination (1%. 1-2%). The lower middle income country had the highest prevalence (6%. 2-12%) as well as the African region (10%. 7-13%). The highest infection rate (4%. 2-7%) was detected in the 1-25 mean age group.

Regular anthelmintic treatment of cats and dogs, and removal of animal feces from public places must be considered 1).


Badri M, Eslahi AV, Olfatifar M, Dalvand S, Houshmand E, Abdoli A, Majidiani H, Eslami A, Zibaei M, Johkool MG, Taghipour A, Hashemipour S. Keys to Unlock the Enigma of Ocular Toxocariasis: A Systematic Review and Meta-analysis. Ocul Immunol Inflamm. 2021 Apr 28:1-12. doi: 10.1080/09273948.2021.1875007. Epub ahead of print. PMID: 33909531.

Cerebral cavernous malformation treatment

Cerebral cavernous malformation treatment

Ren et al. demonstrated that cerebral cavernous malformation (CCM) growth requires increased PI3K/AKT/mTOR pathway and loss of CCM protein function. They identified PIK3CA gain of function (GOF) and CCM loss of function (LOF) somatic mutations in the same cells in a majority of human CCMs. Using mouse models, they showed that CCM growth requires both PI3K GOF and CCM LOF in endothelial cells, and that both CCM LOF and increased expression of the transcription factor KLF4, a downstream MEKK3 effector, augment mTOR signalling in endothelial cells. Consistent with these findings, the mTORC1 inhibitor Rapamycin effectively blocks CCM formation in mouse models. They established a three-hit mechanism analogous to cancer in which aggressive vascular malformations arise through the loss of vascular “suppressor genes” that constrain vessel growth and gain of a vascular “oncogene” that stimulates excess vessel growth. These findings suggest that aggressive CCMs may be treated using clinically approved mTORC1 inhibitors 1).

see Intracranial cavernous malformation surgery.

There have been few comparative studys of microsurgical excision vs conservative treatment of cerebral cavernous malformations (CCM) and none of them has reliably demonstrated a statistically and clinically significant difference.

A prospective, population-based study to identify and independently validate definite cerebral cavernous malformation diagnoses first made in 1999-2003 in Scottish adult residents, used multiple sources of prospective follow-up to assess adults’ dependence and to identify and independently validate outcome events.

Moultrie et al., used univariate and multivariable survival analyses to test the influence of CCM excision on outcome, adjusted for prognostic factors and baseline imbalances.

Of 134 adults, 25 underwent CCM excision; these adults were younger (34 vs 43 years at diagnosis, p = 0.004) and more likely to present with symptomatic intracranial hemorrhage or focal neurological deficit than adults managed conservatively (48% vs 26%; odds ratio 2.7, 95% confidence interval [CI] 1.1-6.5). During 5 years of follow-up, CCM excision was associated with a deterioration to an Oxford Handicap Scale score 2-6 sustained over at least 2 successive years (adjusted hazard ratio [HR] 2.2, 95% CI 1.1-4.3) and the occurrence of symptomatic intracranial hemorrhage or new focal neurologic deficit (adjusted HR 3.6, 95% CI 1.3-10.0).

CCM excision was associated with worse outcomes over 5 years compared to conservative management. Long-term follow-up will determine whether this difference is sustained over patients’ lifetimes. Meanwhile, a randomized controlled trial appears justified.

CLASSIFICATION OF EVIDENCE: This study provides Class III evidence that CCM excision worsens short-term disability scores and increases the risk of symptomatic intracranial hemorrhage and new focal neurologic deficits 2).

Antithrombotic therapy use is associated with a lower risk of intracranial haemorrhage or focal neurological deficit from cerebral cavernous malformations than avoidance of antithrombotic therapy. These findings provide reassurance about safety for clinical practice and require further investigation in a randomised controlled trial 3).


Ren AA, Snellings DA, Su YS, Hong CC, Castro M, Tang AT, Detter MR, Hobson N, Girard R, Romanos S, Lightle R, Moore T, Shenkar R, Benavides C, Beaman MM, Mueller-Fielitz H, Chen M, Mericko P, Yang J, Sung DC, Lawton MT, Ruppert M, Schwaninger M, Körbelin J, Potente M, Awad IA, Marchuk DA, Kahn ML. PIK3CA and CCM mutations fuel cavernomas through a cancer-like mechanism. Nature. 2021 Apr 28. doi: 10.1038/s41586-021-03562-8. Epub ahead of print. PMID: 33910229.

Moultrie F, Horne MA, Josephson CB, Hall JM, Counsell CE, Bhattacharya JJ, Papanastassiou V, Sellar RJ, Warlow CP, Murray GD, Al-Shahi Salman R; Scottish Audit of Intracranial Vascular Malformations (SAIVMs) steering committee and collaborators. Outcome after surgical or conservative management of cerebral cavernous malformations. Neurology. 2014 Aug 12;83(7):582-9. doi: 10.1212/WNL.0000000000000684. Epub 2014 Jul 3. PubMed PMID: 24994841.

Zuurbier SM, Hickman CR, Tolias CS, Rinkel LA, Leyrer R, Flemming KD, Bervini D, Lanzino G, Wityk RJ, Schneble HM, Sure U, Al-Shahi Salman R; Scottish Audit of Intracranial Vascular Malformations Steering Committee. Long-term antithrombotic therapy and risk of intracranial haemorrhage from cerebral cavernous malformations: a population-based cohort study, systematic review, and meta-analysis. Lancet Neurol. 2019 Aug 6. pii: S1474-4422(19)30231-5. doi: 10.1016/S1474-4422(19)30231-5. [Epub ahead of print] PubMed PMID: 31401075.
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