P2-P3 junction aneurysm of the posterior cerebral artery

Aneurysms in the P2 segment arise between the junction of the posterior communicating artery (PCoA) with the PCA and the posterior part of the midbrain. The pterionalsubtemporal, temporopolar, transpetrous and transcortical transchoroidal fissure are the surgical approaches which have been used to gain access to P2 segment aneurysms.

Endovascular coil occlusion has rapidly evolved as a competing therapeutic alternative to surgical clipping in the treatment of P2 segment aneurysms.

However, surgery is still a well-established option for P 2 segment aneurysms and complete closure of the aneurysm can be achieved by surgical clipping 1).

Treatment

Proximal occlusion of PCA represents a treatment option. However, this procedure carries a high risk of ischemic complication

The STA-P3/PTA bypass through the subtemporal approach is a feasible option to maintain blood flow in cases of PCA fusiform aneurysms requiring trapping of the P2 segment 2).


Progressive deconstruction with flow diversion using a Pipeline embolization device (PED; Medtronic) can be utilized to promote thrombosis of broad-based fusiform aneurysms. Current flow diverters require a 0.027-inch microcatheter for deployment. Vakharia et al., presented a patient with a fusiform P2P3 junction posterior cerebral artery aneurysm in which they demonstrate the importance of haptics in microwire manipulation to recognize large-vessel anatomy versus perforator anatomy that may overlap, especially when access is needed in distal tortuous circulations. In addition, the authors demonstrate the need for appropriate visualization before PED deployment. Postembolization runs demonstrated optimal wall apposition with contrast stasis within the aneurysm dome.The video can be found here: https://youtu.be/8kfsSvN3XqM

 3).

References

1)

Zhitao J, Yibao W, Anhua W, Shaowu O, Yunchao B, Renyi Z, Yunjie W. Microsurgical subtemporal approach to aneurysms on the P(2) segment of the posterior cerebral artery. Neurol India. 2010 Mar-Apr;58(2):242-7. doi: 10.4103/0028-3886.63806. PubMed PMID: 20508343.
2)

Kawashima A, Andrade-Barazarte H, Jahromi BR, Oinas M, Elsharkawy A, Kivelev J, Kubota Y, Kawamata T, Hernesniemi JA. Superficial Temporal Artery: Distal Posterior Cerebral Artery Bypass through the Subtemporal Approach: Technical Note and Pilot Surgical Cases. Oper Neurosurg (Hagerstown). 2017 Jun 1;13(3):309-316. doi: 10.1093/ons/opw033. PubMed PMID: 28521345.
3)

Vakharia K, Munich SA, Waqas M, Setlur Nagesh SV, Levy EI. Deployment of distal posterior cerebral artery flow diverter in tortuous anatomy. Neurosurg Focus. 2019 Jan 1;46(Suppl_1):V9. doi: 10.3171/2019.1.FocusVid.18481. PubMed PMID: 30611181.

Middle cerebral artery aneurysm stent assisted coiling

Extra intracranial bypass surgery is a well-established procedure for the treatment of chronic ischemic diseases of the carotid artery. Rarely de novo aneurysms can develop at the site of anastomosis. The treatment of these aneurysms can be very challenging due to various factors, including the presence of graft, previous craniotomyatherosclerosis, and lack of direct access. In a video Joshi et al., from the Department of Neurological Surgery, Rush University Medical CenterLoyola University Medical Center and Cerebrovascular Neurosurgery and Comprehensive Stroke Center, ChicagoIllinois, report and discuss the management of a right middle cerebral artery (MCA) wide-necked de novo aneurysm by stent assisted coiling through a retrograde trans-posterior communicating artery access.The video can be found here: https://youtu.be/MBKolPvOErU

 1).


57 patients with MCA trifurcation wide-necked aneurysms underwent stent-assisted coiling embolization using a solitaire AB stent. All 57 patients completed the surgery successfully. Embolization efficacy was graded according to the Modified Raymond-Roy Classification.

There were 52 cases of complete embolization, 4 cases of residual aneurysm neck, and 1 case of residual aneurysm body. 50 patients participated in a 6-36-month follow-up. There has not been observed any aneurysm rupture and hemorrhage. 50 patients received digital subtraction angiography (DSA) re-examination; 46 patients presenting complete embolization had no aneurysm relapses; 3 patients had residual aneurysm neck demonstrated; 1 patient had no aneurysm neck and others 2 were in stable condition. Finally, the patient with residual aneurysm body showed no sign during follow-up reexamination.

Stent-assisted coiling embolization of intracranial wide-necked aneurysms using the solitaire AB stent was safe and effective 2).


From November 2003 to October 2009, 49 patients (27 men, 22 women; mean age, 52 ± 12 years) harboring 52 complex unruptured MCA aneurysms (11 ruptured previously and coiled but recanalized and 41 unruptured) were treated by EVT by using self-expandable intracranial stents. Procedural complications, clinical outcome, and initial and midterm angiographic results were evaluated. Initial treatment status and aneurysm sac size were tested as potential risk factors for recurrence.

After successful stent deployment, coiling was performed in 50 aneurysms (96.2%) in 47 patients; however, 2 failures (3.8%) occurred in 2 patients. Ten intrastent clot formations (20%) observed on final control angiography induced 2 permanent moderate disabilities (GOS score = 2). Mortality and permanent neurologic morbidity were 0% and 4.3%, respectively. At a mean period of 14 ± 9 months, among 48 aneurysms in 45 patients eligible for follow-up, 34 complete (71%) and 14 partial treatments (29%) were observed, 7 recurrences (14.6%) occurred, and 5 patients (10.4%) needed retreatment. No aneurysm bleeding or symptomatic intrastent stenosis was observed. Aneurysm sac size ≥7 mm and incomplete initial treatment were associated with more recurrences without a statistically significant difference.

For complex unruptured MCA aneurysms, EVT by using a self-expandable intracranial stent was feasible, safe, and durable and could be considered as the first-option treatment 3).

References

1)

Joshi KC, Heiferman DF, Beer-Furlan A, Lopes DK. Stent-assisted coil embolization of MCA aneurysm via a trans-posterior communicating artery access. Neurosurg Focus. 2019 Jan 1;46(Suppl_1):V3. doi: 10.3171/2019.1.FocusVid.18444. PubMed PMID: 30611185.
2)

Chen Y, Zhang Y, Chao YJ, Gao G, Ni CS, Fu XM, Wei JJ, Gu DQ, Yu J. Stent-assisted coiling embolization of middle cerebral artery trifurcation wide-necked aneurysms. Eur Rev Med Pharmacol Sci. 2017 Oct;21(19):4346-4349. PubMed PMID: 29077162.
3)

Vendrell JF, Costalat V, Brunel H, Riquelme C, Bonafe A. Stent-assisted coiling of complex middle cerebral artery aneurysms: initial and midterm results. AJNR Am J Neuroradiol. 2011 Feb;32(2):259-63. doi: 10.3174/ajnr.A2272. Epub 2010 Oct 21. PubMed PMID: 20966055.

Update: Cerebral cavernous malformation pathogenesis

Cerebral cavernous malformation pathogenesis

Genes mutated in cerebral cavernous malformation (CCM) encode proteins that modulate junction formation between vascular endothelial cells.

Most cerebral cavernous malformations are linked to loss-of-function mutations in 1 of 3 genes, namely CCM1 (originally called KRIT1), CCM2(MGC4607), or CCM3 (PDCD10).

How disruption of the CCM complex results in disease remains controversial, with numerous signalling pathways (including Rho, SMAD and Wnt/β-catenin) and processes such as endothelial mesenchymal transition (EndMT) proposed to have causal roles. CCM2 binds to MEKK3 1).

Although a role for these three genes in the formation of these intracranial vascular lesions has been established since the 1990s, additional works have further elucidated the molecular mechanisms by which mutations in these genes and the resultant aberrant proteins interact, leading to the formation of CCMs.

Therefore, it is reasonable to assume that a molecular pathway exists that requires all three proteins to function together correctly for proper cellular function. Moreover, research is demonstrating how each component protein is capable of interacting with numerous other signaling and cytoskeletal molecules allowing for a diverse range of functions in molecular signaling pathways via unique protein–protein interactions.

Significant research findings from 2000 to 2015 have further enhanced our understanding of the pathogenesis of CCM formation. The use of advanced sequencing technologies to characterize genomic mutations and the identification of new signaling pathways and protein–protein interactions have led to great strides in understanding the molecular genetics involved in the development of CCMs. However, many unanswered questions remain, and future studies are clearly needed to improve our understanding of CCM pathogenesis. “Gene to protein to disease” mechanisms involved in the pathogenesis of CCMs should shed further light on potential therapeutic targets. 2).

The Phosphoinositide 3 kinase (PI3K)/Akt pathway is known to play a major role in angiogenesis. Studies have shown that the phosphatase and tensin homologue deleted on chromosome ten (PTEN), a tumor suppressor, is an antagonist regulator of the PI3K/Akt pathway and mediates angiogenesis by activating vascular endothelial growth factor (VEGF) expression.

Understanding the biology of these proteins with respect to their signaling counterpart will help to guide future research towards new therapeutic targets applicable for CCM treatment 3).


Studies identify gain of MEKK3 signalling and KLF2/4 function as causal mechanisms for CCM pathogenesis that may be targeted to develop new CCM therapeutics 4).

CCMs arise from the loss of an adaptor complex that negatively regulates MEKK3KLF2/4 signalling in brain endothelial cells, but upstream activators of this disease pathway have yet to be identified.


Tang et al. identify endothelial Toll-like receptor 4 (TLR4) and the gut microbiome as critical stimulants of cerebral cavernous malformationformation. Activation of TLR4 by Gram negative bacteria or lipopolysaccharide accelerates CCM formation, and genetic or pharmacologic blockade of TLR4 signalling prevents CCM formation in mice. Polymorphisms that increase expression of the TLR4 gene or the gene encoding its co-receptor CD14 are associated with higher CCM lesion burden in humans. Germ-free mice are protected from CCM formation, and a single course of antibiotics permanently alters CCM susceptibility in mice. These studies identify unexpected roles for the microbiome and innate immune signalling in the pathogenesis of a cerebrovascular disease, as well as strategies for its treatment 5).


In this scenario, the lack of effective pharmacologic options remains a critical barrier that poses an unfulfilled and urgent medical need 6).

References

1) , 4)

Zhou Z, Tang AT, Wong WY, Bamezai S, Goddard LM, Shenkar R, Zhou S, Yang J, Wright AC, Foley M, Arthur JS, Whitehead KJ, Awad IA, Li DY, Zheng X, Kahn ML. Cerebral cavernous malformations arise from endothelial gain of MEKK3-KLF2/4 signalling. Nature. 2016 Apr 7;532(7597):122-6. doi: 10.1038/nature17178. Epub 2016 Mar 30. Erratum in: Nature. 2016 May 25;536(7617):488. PubMed PMID: 27027284; PubMed Central PMCID: PMC4864035.
2)

Baranoski JF, Kalani MY, Przybylowski CJ, Zabramski JM. Cerebral Cavernous Malformations: Review of the Genetic and Protein-Protein Interactions Resulting in Disease Pathogenesis. Front Surg. 2016 Nov 14;3:60. Review. PubMed PMID: 27896269.
3)

Kar S, Samii A, Bertalanffy H. PTEN/PI3K/Akt/VEGF signaling and the cross talk to KRIT1, CCM2, and PDCD10 proteins in cerebral cavernous malformations. Neurosurg Rev. 2015 Apr;38(2):229-36; discussion 236-7. doi: 10.1007/s10143-014-0597-8. Epub 2014 Nov 19. PubMed PMID: 25403688.
5)

Tang AT, Choi JP, Kotzin JJ, Yang Y, Hong CC, Hobson N, Girard R, Zeineddine HA, Lightle R, Moore T, Cao Y, Shenkar R, Chen M, Mericko P, Yang J, Li L, Tanes C, Kobuley D, Võsa U, Whitehead KJ, Li DY, Franke L, Hart B, Schwaninger M, Henao-Mejia J, Morrison L, Kim H, Awad IA, Zheng X, Kahn ML. Endothelial TLR4 and the microbiome drive cerebral cavernous malformations. Nature. 2017 May 10. doi: 10.1038/nature22075. [Epub ahead of print] PubMed PMID: 28489816.
6)

Chohan MO, Marchiò S, Morrison LA, Sidman RL, Cavenee WK, Dejana E, Yonas H, Pasqualini R, Arap W. Emerging Pharmacologic Targets in Cerebral Cavernous Malformation and Potential Strategies to Alter the Natural History of a Difficult Disease: A Review. JAMA Neurol. 2018 Nov 26. doi: 10.1001/jamaneurol.2018.3634. [Epub ahead of print] PubMed PMID: 30476961.

Applied Cranial-Cerebral Anatomy: Brain Architecture and Anatomically Oriented Microneurosurgery

Applied Cranial-Cerebral Anatomy: Brain Architecture and Anatomically Oriented Microneurosurgery


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This book is the first to offer a comprehensive guide to understanding the brain’s architecture from a topographical viewpoint. Authored by a leading expert in surgical neuroanatomy, this practical text provides tri-dimensional understanding of the cerebral hemispheres, and the relationships between cerebral surfaces and the skull’s outer surfaces through detailed brain dissections and actual clinical cases with operative photographs and correlative neuroimaging. For neurosurgeons, neuroradiologists and neurologists at all levels, this book emphasises the anatomy of the sulci and gyri of the cerebral surface. It is an essential resource for the general neurosurgery practice, and more particularly for planning surgical access routes for intracranial tumors.
 

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Update: Familial cerebral cavernous malformation

Familial cerebral cavernous malformation

Familial cerebral cavernous malformations, which account for at least 20% of all cases, can be passed from parent to child. Individuals with familial CCMs typically have multiple lesions. Familial CCMs are passed through families in an autosomal dominant manner, which means one copy of the altered gene in each cell is sufficient to cause the disorder. Each child of an individual with familial CCM has a 50% chance of inheriting the mutation.
It is an autosomal-dominant disease with incomplete penetrance. The pathogenic genes of FCCM have been mapped into three loci: CCM1/KRIT1, CCM2/MGC4607, and CCM3/PDCD10.
see https://www.ncbi.nlm.nih.gov/books/NBK1293/.


Although the clinical course is unpredictable, symptoms typically present during adult life and include headaches, focal neurological deficits, seizures, and potentially fatal stroke. In addition to neural lesions, extraneural cavernous malformations have been described in familial disease in several tissues, in particular the skin 1).


In recent years there has been an increasing amount of publications linking FCCMs with other pathology, predominantly with extracranial and intracranial mesenchymal anomalies.
When faced with an unusual clinical feature in a patient with a Mendelian disorder, the clinician may entertain the possibilities of either the feature representing a novel manifestation of that disorder or the co-existence of a different inherited condition. Here we describe an individual with a submandibular oncocytoma, pulmonary bullae and renal cysts as well as multiple cerebral cavernous malformations and haemangiomas. Genetic investigations revealed constitutional mutations in FLCN, associated with Birt-Hogg-Dubé syndrome (BHD) and CCM2, associated with familial cerebral cavernous malformation. Intracranial vascular pathologies (but not cerebral cavernous malformation) have recently been described in a number of individuals with BHD (Kapoor et al. in Fam Cancer 14:595-597, 10.1007/s10689-015-9807-y , 2015) but it is not yet clear whether they represent a genuine part of that conditions’ phenotypic spectrum. We suggest that in such instances of potentially novel clinical features, more extensive genetic testing to consider co-existing conditions should be considered where available. The increased use of next generation sequencing applications in diagnostic settings is likely to lead more cases such as this being revealed 2).


A study described an unusual association between 2 independent hereditary diseases of confirmed genetic origin-a combination that has not been described previously 3).
Rosário Marques et al. documented a novel mutation on KRIT1 gene, and the second to be reported in a Portuguese family. This mutation consists in a two nucleotide insertion (c.947_948insAC) within the exon 10, resulting in premature protein termination (p.Leu317Argfs*2). These findings will hopefully contribute to a better clinical, imaging and genetic characterisation of this disease, particularly while trying to identify the factors that influence its treatment and prognosis 4).


Yang et al., investigated the genetic mutation in a Chinese family with FCCM.
The proband is a 29-year-old female presenting with a 1-month history of headache. Brain magnetic resonance imaging (MRI) revealed multiple intracranial lesions, the largest one showing a popcorn-like appearance. After a 4-year conservative observation, there was no significant clinical or radiological progression. Family investigation found five of her relatives had multiple CCM lesions. DNA sequencing analysis in the proband disclosed a novel heterozygous deletion mutation (c.1919delT; p.Phe640SerfsX21) in exon 17 of the CCM1/KRIT1 gene. This mutation leads to a frameshift and is predicted to cause a premature termination codon to generate a truncated Krev interaction trapped-1 (Krit1) protein of 659 amino acids. The mutation segregated with the disease in the family. C The current study identified a novel CCM1/KRIT1 heterozygous deletion mutation (c.1919delT) associated with FCCM. The findings expand the CCM gene mutation profiles in the Chinese population, which will be beneficial for genetic counseling 5).


A proband was hospitalized for sudden unconsciousness and underwent surgical treatment. The section of lesions showed classical cavernous-dilated vessels without intervening brain parenchyma, and hemosiderin-laden macrophages were accumulated in the surrounding tissue. In addition, magnetic resonance imaging (MRI) showed severe multiple cerebral cavernous malformation (CCM) lesions in cerebrum, brainstem, and cerebellum in other affected subjects. Especially, for the proband’s mother, hundreds of lesions were presented, and a few lesions were found in the expanded lateral ventricle (Evans’ index =0.33). Moreover, she showed the similar symptoms of hydrocephalus, including headache, dizziness, and diplopia. It was extremely rare in previous reports. To date, the genetic alterations leading to FCCM in Chinese population remain largely unknown. We investigated genetic defects of this family. Sequence analyses disclosed a novel heterozygous insertion mutation (c.1896_1897insT; p.Pro633SerfsTer22) in KRIT1/CCM1. Moreover, our real-time PCR results revealed that the mRNA level of KRIT1/CCM1 were significantly decreased in FCCM subjects (CCM family =0.42 ± 0.20 vs. healthy control =1.01 ± 0.16, P = 0.004). It indicated that this mutation could cause KRIT1/CCM1 functional mRNA deficiency. It may be closely related with the pathogenesis of FCCM. Our findings provided a new gene mutation profile which will be of great significance in early diagnosis and appropriate clinical surveillance of FCCM patients 6).

Case series

Fifty-seven familial CCM type-1 patients were included in this institutional review board-approved study. Baseline SWI (n = 57) and follow-up SWI (n = 17) were performed on a 3T Siemens MR scanner with lesions counted manually by the study neuroradiologist. We modified an algorithm for detecting radiation-induced microbleeds on SWI images in brain tumor patients, using a training set of 22 manually delineated CCM microbleeds from two random scans. Manual and automated counts were compared using linear regression with robust standard errors, intra-class correlation (ICC), and paired t tests. A validation analysis comparing the automated counting algorithm and a consensus read from two neuroradiologists was used to calculate sensitivity, the proportion of microbleeds correctly identified by the automated algorithm. RESULTS: Automated and manual microbleed counts were in strong agreement in both baseline (ICC = 0.95, p < 0.001) and longitudinal (ICC = 0.88, p < 0.001) analyses, with no significant difference between average counts (baseline p = 0.11, longitudinal p = 0.29). In the validation analysis, the algorithm correctly identified 662 of 1325 microbleeds (sensitivity=50%), again with strong agreement between approaches (ICC = 0.77, p < 0.001). CONCLUSION: The automated algorithm is a consistent method for counting microbleeds in familial CCM patients that can facilitate lesion quantification and tracking 7).


The authors retrospectively reviewed abdominal CT scans in 38 patients with fCCM, 38 unaffected age- and sex-matched control subjects, and 13 patients with sporadic, nonfamilial cerebral cavernous malformation (CCM). The size, number, and laterality of calcifications and the morphologic characteristics of the adrenal gland were recorded. Brain lesion count was recorded from brain magnetic resonance (MR) imaging in patients with fCCM. The prevalence of adrenal calcifications in patients with fCCM was compared with that in unaffected control subjects and those with sporadic CCM by using the Fisher exact test. Additional analyses were performed to determine whether age and brain lesion count were associated with adrenal findings in patients with fCCM. Results Small focal calcifications (SFCs) (≤5 mm) were seen in one or both adrenal glands in 19 of the 38 patients with fCCM (50%), compared with 0 of the 38 unaffected control subjects (P < .001) and 0 of the 13 subjects with sporadic CCM (P = .001). Adrenal calcifications in patients with fCCM were more frequently left sided, with 17 of 19 patients having more SFCs in the left adrenal gland than the right adrenal gland and 50 of the 61 observed SFCs (82%) found in the left adrenal gland. No subjects had SFCs on the right side only. In patients with fCCM, the presence of SFCs showed a positive correlation with age (P < .001) and number of brain lesions (P < .001). Conclusion Adrenal calcifications identified on CT scans are common in patients with fCCM and may be a clinically silent manifestation of disease 8).
1)

de Vos IJ, Vreeburg M, Koek GH, van Steensel MA. Review of familial cerebral cavernous malformations and report of seven additional families. Am J Med Genet A. 2017 Feb;173(2):338-351. doi: 10.1002/ajmg.a.38028. Epub 2016 Oct 28. Review. PubMed PMID: 27792856.
2)

Whitworth J, Stausbøl-Grøn B, Skytte AB. Genetically diagnosed Birt-Hogg-Dubé syndrome and familial cerebral cavernous malformations in the same individual: a case report. Fam Cancer. 2017 Jan;16(1):139-142. doi: 10.1007/s10689-016-9928-y. PubMed PMID: 27722904; PubMed Central PMCID: PMC5243871.
3)

Belousova OB, Okishev DN, Ignatova TM, Balashova MS, Boulygina ES. Hereditary Multiple Cerebral Cavernous Malformations Associated with Wilson Disease and Multiple Lipomatosis. World Neurosurg. 2017 Sep;105:1034.e1-1034.e6. doi: 10.1016/j.wneu.2017.06.002. Epub 2017 Jun 8. PubMed PMID: 28602929.
4)

Rosário Marques I, Antunes F, Ferreira N, Grunho M. Familial cerebral cavernous malformation: Report of a novel KRIT1 mutation in a Portuguese family. Seizure. 2017 Nov 10;53:72-74. doi: 10.1016/j.seizure.2017.10.020. [Epub ahead of print] PubMed PMID: 29145060.
5)

Yang C, Wu B, Zhong H, Li Y, Zheng X, Xu Y. A novel CCM1/KRIT1 heterozygous deletion mutation (c.1919delT) in a Chinese family with familial cerebral cavernous malformation. Clin Neurol Neurosurg. 2017 Nov 20;164:44-46. doi: 10.1016/j.clineuro.2017.11.005. [Epub ahead of print] PubMed PMID: 29169046.
6)

Wang H, Pan Y, Zhang Z, Li X, Xu Z, Suo Y, Li W, Wang Y. A Novel KRIT1/CCM1 Gene Insertion Mutation Associated with Cerebral Cavernous Malformations in a Chinese Family. J Mol Neurosci. 2017 Feb;61(2):221-226. doi: 10.1007/s12031-017-0881-5. Epub 2017 Feb 3. PubMed PMID: 28160210.
7)

Zou X, Hart BL, Mabray M, Bartlett MR, Bian W, Nelson J, Morrison LA, McCulloch CE, Hess CP, Lupo JM, Kim H. Automated algorithm for counting microbleeds in patients with familial cerebral cavernous malformations. Neuroradiology. 2017 Jul;59(7):685-690. doi: 10.1007/s00234-017-1845-8. Epub 2017 May 22. PubMed PMID: 28534135; PubMed Central PMCID: PMC5501247.
8)

Strickland CD, Eberhardt SC, Bartlett MR, Nelson J, Kim H, Morrison LA, Hart BL. Familial Cerebral Cavernous Malformations Are Associated with Adrenal Calcifications on CT Scans: An Imaging Biomarker for a Hereditary Cerebrovascular Condition. Radiology. 2017 Aug;284(2):443-450. doi: 10.1148/radiol.2017161127. Epub 2017 Mar 20. PubMed PMID: 28318403; PubMed Central PMCID: PMC5519414.

Update: Anterior cerebral artery infarct

Anterior cerebral artery infarct

Stroke in the anterior cerebral artery territory are much less common than either middle cerebral artery or posterior cerebral artery territory infarcts.

Epidemiology

ACA territory infarcts are rare, comprising ~2% of ischaemic strokes.
ACA territory infarcts are less common because if the A1 segment is occluded there is generally enough collateral flow via the contralateral A1 segment to supply the distal ACA territory.

Etiology

Embolic strokes (often with MCA involvement) are the most common cause.
Rarely, they are also seen as a complication of severe midline shift, where the ACA is occluded by mass effect or severe vasospasm.
An asymmetry of the A1 segment of the anterior cerebral artery (A1SA) was identified on digital subtraction angiography studies from 127 patients (21.4%) and was strongly associated with anterior communicating artery aneurysm (ACoAA) (p < 0.0001, OR 13.7). An A1SA independently correlated with the occurrence of ACA infarction in patients with ACoAA (p = 0.047) and in those without an ACoAA (p = 0.015). Among patients undergoing Anterior communicating artery aneurysm endovascular treatment, A1SA was independently associated with the severity of ACA infarction (p = 0.023) and unfavorable functional outcome (p = 0.045, OR = 2.4).
An A1SA is a common anatomical variation in SAH patients and is strongly associated with ACoAA. Moreover, the presence of A1SA independently increases the likelihood of ACA infarction. In SAH patients undergoing ACoAA coiling, A1SA carries the risk for severe ACA infarction and thus an unfavorable outcome. Clinical trial registration no.: DRKS00005486 (http://www.drks.de/) 1).

Clinical features

Diagnosis

The features are those of cerebral infarction in the anterior cerebral artery vascular territory:
Paramedian frontoparietal cerebral cortex
Anterior corpus callosum.
Anterior limb of the internal capsule.
Inferior portion of the Caudate nucleus head.

Differential diagnosis

Case series

Kumral et al. studied 48 consecutive patients who admitted to the stroke unit over a 6-year period.
They performed magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) in all patients, and Diffusion weighted magnetic resonance imaging (DWI) in 21. In the stroke registry, patients with ACA infarction represented 1.3% of 3705 patients with ischemic stroke. The main risk factors of ACA infarcts was hypertension in 58% of patients, diabetes mellitus in 29%, hypercholesterolemia in 25%, cigarette smoking in 19%, atrial fibrillation in 19%, and myocardial infarct in 6%. Presumed causes of ACA infarct were large-artery disease and cardioembolism in 13 patients each, small-artery disease (SAD) in the territory of Heubner’s artery in two and atherosclerosis of large-arteries (<50% stenosis) in 16. On clinico-radiologic analysis there were three main clinical patterns depending on lesion side; left-side infarction (30 patients) consisting of mutism, transcortical motor aphasia, and hemiparesis with lower limb predominance; right side infarction (16 patients) accompanied by acute confusional state, motor hemineglect and hemiparesis; bilateral infarction (two patients) presented with akinetic mutism, severe sphincter dysfunction, and dependent functional outcome. Our findings suggest that clinical and etiologic spectrum of ACA infarction may present similar features as that of middle cerebral artery infarction, but frontal dysfunctions and callosal syndromes can help to make a clinical differential diagnosis. Moreover, at the early phase of stroke, DWI is useful imaging method to locate and delineate the boundary of lesion in the territory of ACA 3).
1)

Jabbarli R, Reinhard M, Roelz R, Kaier K, Weyerbrock A, Taschner C, Scheiwe C, Shah M. Clinical relevance of anterior cerebral artery asymmetry in aneurysmal subarachnoid hemorrhage. J Neurosurg. 2017 Nov;127(5):1070-1076. doi: 10.3171/2016.9.JNS161706. Epub 2016 Dec 23. PubMed PMID: 28009232.
3)

Kumral E, Bayulkem G, Evyapan D, Yunten N. Spectrum of anterior cerebral artery territory infarction: clinical and MRI findings. Eur J Neurol. 2002 Nov;9(6):615-24. PubMed PMID: 12453077.

Update: Middle cerebral artery aneurysm endovascular treatment with Flow Diverter

Middle cerebral artery aneurysm endovascular treatment with Flow Diverter

Flow diverter for middle cerebral artery aneurysm treatment should be considered an alternative when traditional treatment methods are not feasible 1).
When performed in a select treatment group, high rates of aneurysm occlusion and protection against re-rupture can be achieved 2).
Longer angiographic follow-ups are needed to assess the morphologic outcome; immediate subtotal occlusions do not seem to be related to rupture 3).
Findings suggest that complete occlusion after endovascular treatment with FDD can be delayed (>6 months). Ischemic complications may occur as early or delayed, particularly at clopidogrel interruption 4).
The Pipeline Embolization Device provides a safe and effective treatment alternative for wide-neck MCA aneurysms that give rise to a bifurcating or distal branch when other endovascular techniques are thought to be unfeasible or more risky 5).
WEB flow disruption seems to be a promising technique for the treatment of complex MCA aneurysms, particularly those with a wide neck or unfavorable dome-to-neck ratio 6).
For Caroff et al. compared with other available therapeutic options, the flow-diverter stent does not appear to be a suitable solution for the treatment of saccular MCA bifurcation aneurysms 7).
Unsatisfactory occlusion rate in bifurcation aneurysms likely results from residual filling of the aneurysms in cases in which the jailed side branch remains patent 8).

Systematic review and meta-analysis

A systematic search of PubMed, MEDLINE, and Embase was performed for studies published from 2008 to May 2017.
According to the Preferred Reporting Items for Systematic Reviews and MetaAnalyses, Cagnazzo et al. selected studies with >5 patients describing angiographic and clinical outcomes after flow-diversion treatment of MCA aneurysms.
Random-effects metaanalysis was used to pool the following outcomes: aneurysm occlusion rate, procedure-related complications, rupture rate of treated aneurysms, and occlusion of the jailed branches.
Twelve studies evaluating 244 MCA aneurysms were included in this meta-analysis. Complete/near-complete occlusion was obtained in 78.7% (95% CI, 67.8%-89.7%) of aneurysms. The rupture rate of treated aneurysms during follow-up was 0.4% per aneurysm-year. The rate of treatment-related complications was 20.7% (95% CI, 14%-27.5%), and approximately 10% of complications were permanent. The mortality rate was close to 2%. Nearly 10% (95% CI, 4.7%-15.5%) of jailed arteries were occluded during follow-up, whereas 26% (95% CI, 14.4%-37.6%) had slow flow. Rates of symptoms related to occlusion and slow flow were close to 5%.
Small and retrospective series could affect the strength of the reported results.
Given the not negligible rate of treatment-related complications, flow diversion for MCA aneurysms should be considered an alternative treatment when traditional treatment methods are not feasible. However, when performed in this select treatment group, high rates of aneurysm occlusion and protection against re-rupture can be achieved 9).

Case series

2017

Consecutive patients treated from January 2010 to December 2014 by Iosif et al. by using endovascular flow-diverting stents for MCA bifurcation aneurysms were evaluated retrospectively with prospectively maintained data. All patients had been followed for at least 12 months after treatment, with at least 2 control angiograms; regional flow-related angiographic modifications were registered by using a new angiographic outcome scale for flow diverters. Data were analyzed with emphasis on procedure-related events, angiographic results, and clinical outcome.
Fifty-eight patients were included in the study, with 63 MCA bifurcation aneurysms; 13 of these were large and giant. Pretreatment mRS was 0 for 12 patients (20.7%), 1 for 41 (70.7%), and 2 for 5 patients (8.6%). Six-month control revealed mRS 0-2 for 57 (98.3%) patients and 3 for 1 (1.7%) patient. Procedure-related morbidity and mortality were 8.6% (5/58) and 0%, respectively. From 95% of still circulating immediate postprocedure angiographic outcomes, 68% progressed to aneurysm occlusion at 6 months and 95%, to occlusion at 12 months, with a 0% aneurysm rupture rate.
Flow diverters seem to be an effective treatment alternative for complex MCA bifurcation aneurysms, with reasonable complication rates. Longer angiographic follow-ups are needed to assess the morphologic outcome; immediate subtotal occlusions do not seem to be related to rupture 10).


Bhogal et al. retrospectively reviewed there prospectively maintained database to collect information for all patients with unruptured saccular bifurcation MCA aneurysms treated with FDS between January 2010 and January 2016. In addition to demographic data, they recorded the location, aneurysm characteristics, previous treatments, number and type of FDS, complications, and clinical and angiographic follow-up.
The search identified 13 patients (7 males) with an average age of 61.7 years (47-74 years). All patients had a single bifurcation aneurysm of the MCA, and none of the aneurysms were acutely ruptured. The average fundus size of the saccular aneurysms was 3 mm (range 1.5-10 mm). Follow-up studies were available for 12 patients. Based on the most recent follow-up angiograms, six aneurysms (50%) were totally occluded; five aneurysms (41.7%) showed only a small remnant; and one aneurysm (8.3%) remained unchanged. One patient suffered from an ischemic stroke with resultant permanent hemiparesis (mRS 3). In another case, there was an in-stent thrombosis during the intervention, which resolved upon intra-arterial infusion of Eptifibatide (mRS 0). There were no intra-operative vessel or aneurysm ruptures and no mortalities. Angiography of the covered MCA branches showed no change in the caliber or flow of the vessel in six (50%), a reduction in caliber in five (41.7%), and a complete occlusion in one (8.3%). All caliber changes and occlusions of the vessels were asymptomatic.
91.7% of treated MCA bifurcation aneurysms were either completely occluded or showed only a small remnant with a good safety profile. Flow diversion of MCA bifurcation aneurysms should be considered as an alternative treatment strategy when microsurgical clipping or alternative endovascular treatment options are not feasible 11).

2016

Patients with MCAAs were treated by flow diversion if surgical or other endovascular treatment modalities had failed or were deemed likely to fail. Angiographic and clinical outcome of these patients was assessed retrospectively. Aneurysm location on MCA was defined as M1 segment, “true bifurcation” (classical bifurcation of MCA into superior and inferior trunks), “variant bifurcation” (bifurcation of early frontal or early/distal temporal branches), or M2 segment. Aneurysm morphology was classified as saccular versus dissecting/fusiform.
Treatment was attempted in 29 MCAAs. Technical failure rate was 3.4% (1/29). Thirteen of aneurysms were fusiform. Of the bifurcation aneurysms, most (10/16) were the variant type. Overall and procedure-related mortality/permanent morbidity rates were 10.3% (3/29) and 3.5% (1/29). Total occlusion rates (mean angiographic follow-up 10.3 months) for saccular and fusiform aneurysms were 40% and 75%, respectively. In bifurcation aneurysms, occlusion was strongly associated with side-branch occlusion (P < 0.005).
In this series, flow diversion for the treatment of MCAAs was safe, was effective in the treatment of fusiform MCAAs, and was not as effective at mid-term for MCA bifurcation aneurysms. Unsatisfactory occlusion rate in bifurcation aneurysms likely results from residual filling of the aneurysms in cases in which the jailed side branch remains patent 12).


Fourteen patients with 15 aneurysms were included in the study. Ischemic complications, as confirmed by MR imaging, occurred in 6 patients (43%). Procedure-related morbidity and mortality at last follow-up were 21% and 0%, respectively. Angiographic follow-up was available for 13 aneurysms, with a mean follow-up of 16 months. Complete occlusion was obtained for 8 aneurysms (62%).
Compared with other available therapeutic options, the flow-diverter stent does not appear to be a suitable solution for the treatment of saccular MCA bifurcation aneurysms 13).


From February 2010 to December 2013, 14 patients (10 women; mean age 59 years) with 15 small MCA aneurysms were treated with FDD. All procedures were performed with the Pipeline embolization device (PED).
Complete occlusion was obtained in 12/15 aneurysms (80%) and partial occlusion in 3 (20%). Among 13 aneurysms with a side branch, this was patent at the angiographic control in 4 cases, showed decreased filling in 6, and was occluded in 3 (with neurological deficits in 2). All PEDs were patent at follow-up. Post-procedural ischemic complications occurred in 4 (27%) procedures with permanent neurological deficit (modified Rankin score 2) in 3 (21%). No early or delayed aneurysm rupture, no subarachnoid or intraparenchymal hemorrhage and no deaths occurred.
Endovascular treatment with FDD is a relatively safe treatment for small MCA aneurysms resulting in a high occlusion rate. The findings suggest that complete occlusion after endovascular treatment with FDD can be delayed (>6 months). Ischemic complications may occur as early or delayed, particularly at clopidogrel interruption 14).

2014

Twenty-five aneurysms located at the MCA bifurcation (n = 21) or distal (n = 4) were treated. Of these, 22 were small and 3 were large. A single device was used in all but 2. No deaths occurred in the series. All patients had at least 1 control angiographic study, 21 of which were DSA (3-30 months), which showed that 12 of the rising branches were patent whereas 6 were filling in reduced caliber and 3 were occluded asymptomatically. According to the last angiographic follow-up, complete occlusion was revealed in 21 of 25 aneurysms (84%).
The Pipeline Embolization Device provides a safe and effective treatment alternative for wide-neck MCA aneurysms that give rise to a bifurcating or distal branch when other endovascular techniques are thought to be unfeasible or more risky 15).

2013

Thirty-three patients with 34 MCA aneurysms were treated with the Woven EndoBridge (WEB) in 5 European centers. The ability to successfully deploy the WEB, procedure- and device-related adverse events, morbidity and mortality of the treatment, and short-term angiographic follow-up results were analyzed.
Most treated aneurysms were unruptured (85.3%) and were between 5 and 10 mm (85.3%) with a neck size ≥  4 mm (88.2%). The treatment failed in 1 of the 34 aneurysms (2.9%) owing to a lack of appropriate device size. Treatment was performed exclusively with the WEB in 29 of 33 aneurysms (87.9%). Additional treatment (coiling and/or stenting) was used in 4 of 33 aneurysms (12.1%). Mortality of the treatment was 0.0% and morbidity was 3.1% (intraoperative rupture with modified Rankin Scale score of 3 at the 1-month follow-up). In short-term follow-up (range, 2-12 months), adequate occlusion (total occlusion or neck remnant) was observed in 83.3% of aneurysms.
WEB flow disruption seems to be a promising technique for the treatment of complex MCA aneurysms, particularly those with a wide neck or unfavorable dome-to-neck ratio 16).

Case reports

Burrows et al. present the case of an adolescent with a middle cerebral artery (MCA) fusiform aneurysm which recurred following clip reconstruction and bypass. The aneurysm was successfully treated with endovascular flow diversion 17).
1) , 11)

Bhogal P, AlMatter M, Bäzner H, Ganslandt O, Henkes H, Aguilar Pérez M. Flow Diversion for the Treatment of MCA Bifurcation Aneurysms-A Single Centre Experience. Front Neurol. 2017 Feb 2;8:20. doi: 10.3389/fneur.2017.00020. eCollection 2017. PubMed PMID: 28210239; PubMed Central PMCID: PMC5288345.
2) , 9)

Cagnazzo F, Mantilla D, Lefevre PH, Dargazanli C, Gascou G, Costalat V. Treatment of Middle Cerebral Artery Aneurysms with Flow-Diverter Stents: A Systematic Review and Meta-Analysis. AJNR Am J Neuroradiol. 2017 Oct 5. doi: 10.3174/ajnr.A5388. [Epub ahead of print] PubMed PMID: 28982785.
3) , 10)

Iosif C, Mounayer C, Yavuz K, Saleme S, Geyik S, Cekirge HS, Saatci I. Middle Cerebral Artery Bifurcation Aneurysms Treated by Extrasaccular Flow Diverters: Midterm Angiographic Evolution and Clinical Outcome. AJNR Am J Neuroradiol. 2017 Feb;38(2):310-316. doi: 10.3174/ajnr.A5022. Epub 2016 Dec 15. PubMed PMID: 27979794.
4) , 14)

Briganti F, Delehaye L, Leone G, Sicignano C, Buono G, Marseglia M, Caranci F, Tortora F, Maiuri F. Flow diverter device for the treatment of small middle cerebral artery aneurysms. J Neurointerv Surg. 2016 Mar;8(3):287-94. doi: 10.1136/neurintsurg-2014-011460. Epub 2015 Jan 20. PubMed PMID: 25603808.
5) , 15)

Yavuz K, Geyik S, Saatci I, Cekirge HS. Endovascular treatment of middle cerebral artery aneurysms with flow modification with the use of the pipeline embolization device. AJNR Am J Neuroradiol. 2014 Mar;35(3):529-35. doi: 10.3174/ajnr.A3692. Epub 2013 Sep 26. PubMed PMID: 24072620.
6) , 16)

Pierot L, Klisch J, Cognard C, Szikora I, Mine B, Kadziolka K, Sychra V, Gubucz I, Januel AC, Lubicz B. Endovascular WEB flow disruption in middle cerebral artery aneurysms: preliminary feasibility, clinical, and anatomical results in a multicenter study. Neurosurgery. 2013 Jul;73(1):27-34; discussion 34-5. doi: 10.1227/01.neu.0000429860.04276.c1. PubMed PMID: 23615104.
7) , 13)

Caroff J, Neki H, Mihalea C, D’Argento F, Abdel Khalek H, Ikka L, Moret J, Spelle L. Flow-Diverter Stents for the Treatment of Saccular Middle Cerebral Artery Bifurcation Aneurysms. AJNR Am J Neuroradiol. 2016 Feb;37(2):279-84. doi: 10.3174/ajnr.A4540. Epub 2015 Sep 24. PubMed PMID: 26405085.
8) , 12)

Topcuoglu OM, Akgul E, Daglioglu E, Topcuoglu ED, Peker A, Akmangit I, Belen D, Arat A. Flow Diversion in Middle Cerebral Artery Aneurysms: Is It Really an All-Purpose Treatment? World Neurosurg. 2016 Mar;87:317-27. doi: 10.1016/j.wneu.2015.11.073. Epub 2015 Dec 23. PubMed PMID: 26723288.
17)

Burrows AM, Zipfel G, Lanzino G. Treatment of a pediatric recurrent fusiform middle cerebral artery (MCA) aneurysm with a flow diverter. J Neurointerv Surg. 2013 Nov;5(6):e47. doi: 10.1136/neurintsurg-2012-010478.rep. Epub 2012 Nov 27. PubMed PMID: 23188788.

Flow Diversion of Cerebral Aneurysms

Flow Diversion of Cerebral Aneurysms
By Min S. Park, Philipp Taussky, Felipe C. Albuquerque, Cameron G. McDougal

Flow Diversion of Cerebral Aneurysms

List Price: $149.99
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From detachable balloons and GDC coils to the recent advent of flow diversion, practitioners of have endovascular neurosurgery been fortunate to work in an era of rapid and exciting advances. The first commercially available flow diverter in the U.S. was approved specifically for a small subset of cerebral aneurysms. Recent experience has demonstrated its utility in treating challenging or otherwise untreatable aneurysms, safely and efficaciously. The design of these devices requires learning radically different methods than those used in the deployment of other, non-braided stents.
Flow Diversion of Cerebral Aneurysms by Min Park, Philipp Taussky, Felipe Albuquerque, and Cameron McDougall provides step-by-step guidance on utilization of flow diversion technology in clinical practice. Reflecting the combined experience and knowledge of pioneers in neurointerventional surgery, this comprehensive book fills a gap in available resources. Twenty-one chapters cover fundamentals to advanced concepts – historical perspective to future developments.
Key Features

  • More than 250 high quality graphics and illustrative case studies reinforce key concepts
  • Techniques and nuances of Pipeline, Silk (Balt Extrusion), Surpass Streamline, and Flow-Redirection Endoluminal Device (FRED) deployment
  • An overview of current flow diversion devices, discussion of coil embolization versus flow diversion, off-label uses, adjuvant approaches, and hemodynamic modifications
  • Pharmacology, flow diversion grading scales, and post-procedure radiographic imaging
  • Clinical pearls on ruptured aneurysms, intraprocedural/postprocedural complications, and management of aneurysm residuals

The ultimate goal of incorporating cutting-edge flow diversion techniques into the aneurysm treatment paradigm is improved efficacy and patient outcome. The knowledge gleaned from this outstanding resource will help residents and fellows learn to deploy flow diverters for the first time and enable seasoned clinicians to expand their neurointerventional radiology skills.


Product Details

  • Published on: 2017-10-25
  • Original language: English
  • Dimensions: 8.50″ h x .0″ w x 11.00″ l,
  • Binding: Hardcover
  • 176 pages
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