Unruptured anterior communicating artery aneurysm treatment

Unruptured anterior communicating artery aneurysm treatment

see also Anterior communicating artery aneurysm treatment.


The risk associated with treating unruptured anterior communicating artery aneurysms in patients age <65 years is low. Comparing risk with natural history studies, these patients can be expected to outperform natural history within 5 years. Recognizing the risk of smaller anterior communicating artery aneurysms, these findings suggest that treatment of even small lesions may be beneficial 1).


Anterior communicating artery aneurysm treatment requires more collaboration between microsurgical clipping and endovascular therapy. Evaluation of patient and anterior communicating artery aneurysm characteristics by considering the advantages and disadvantages of both techniques could provide an optimal treatment modality. A hybrid vascular neurosurgeon is expected to be a proper solution for the management of these conditions 2).

1)
Schmalz PGR, Enriquez-Marulanda A, Alturki A, Stapleton CJ, Thomas AJ, Ogilvy CS. Combined Outcomes of Endovascular or Surgical Treatment of Unruptured Anterior Communicating Artery Aneurysms: Is a More Aggressive Management Strategy Warranted? World Neurosurg. 2018 Jul;115:e331-e336. doi: 10.1016/j.wneu.2018.04.046. Epub 2018 Apr 17. PMID: 29673817.
2)
Moon JS, Choi CH, Lee TH, Ko JK. Result of coiling versus clipping of unruptured anterior communicating artery aneurysms treated by a hybrid vascular neurosurgeon. J Cerebrovasc Endovasc Neurosurg. 2020 Oct 6. doi: 10.7461/jcen.2020.E2020.06.005. Epub ahead of print. PMID: 33017881.

Middle cerebral artery occlusion

Middle cerebral artery occlusion

Middle cerebral artery stenosis may lead to a middle cerebral artery stroke via three mechanisms:

(1) deep lacunar infarcts that develop when the exiting branch of the lenticulostriate artery is trapped within the thromboatheroma

(2) development of atheromatous ulceration with thrombosis and subsequent distal embolization

(3) hemispheric hypoperfusion caused by significant MCA obstruction and inadequate collateralization

Clinical

Complications

see Malignant middle cerebral artery territory infarction.


In these patients the clinical presentation usually starts with focal signs and progresses with a decline of consciousness until brainstem dysfunction is evident.

A shift of the ischemic tissue rather than intracranial hypertension is the most likely responsible for the initial decrease in consciousness 1) 2).

Several other satellite reactions are involved in an inexorable pathogenetic cascade, including disturbances of microvascular tone, endothelial cell swelling, and activation of platelets, leucocytes, and coagulation 3).

Diagnosis

Imaging studies are the mainstay for identification of people at higher risk for malignant infarction among the ischemic stroke population.

Perfusion computed tomography

Perfusion computed tomography of the brain is routinely performed for first and later controls. The earliest warning signs for developing malignant infarction include involvement of an area larger than 50% of the MCA territory and an infarct extending also to the anterior or posterior cerebral artery territories. A midline shift >10 mm, effacement of subarachnoid spaces, and attenuation of corticomedullary differentiation are also related to higher risk of severe deterioration 4), but they usually occur later, when a malignant syndrome is already in progress. The intravenous injection of contrast medium with elaboration of its distribution (perfusion-CT) entails higher diagnostic accuracy of ischemic areas and an even earlier detection of patients at higher risk. A drop in cerebral perfusion of more 66% is related to a likely malignant evolution 5).

Magnetic resonance imaging

Magnetic resonance imaging is another helpful exam, which in ischemic stroke can be used for prognostic purposes within few hours of clinical onset. Its sensitivity is higher than CT and it is more likely to show changes at earlier time points than CT scan. On diffusion weighted images (DWI) an ischemic area of at least 145 mL strongly predicts a massive cerebral infarction 6) 7).

It is straightforward that at final stages the pressure inside the skull of patients with large cerebral infarction is probably high. Anyway, a pressure increase limited to the infarcted and immediately adjacent areas could happen, leading to neurological worsening and even death despite no spread of intracranial hypertension 8).

Undisputed poor prognosis predictors as CT uncal herniation and anisocoria sometimes occur without an overall ICP raise is detected 9).

The measurement may also be influenced by the device used (solid-state or fluid-filled) as well as by its location (subdural, intraparenchymal, intraventricular; ipsilateral or contralateral to ischemia) 10).

Treatment

see Middle cerebral artery occlusion treatment.

Outcome

Malignant evolution is more common in younger patients 11).

Despite optimal medical management this condition may lead to death in 70–80% of cases 12) 13).

The criteria for surgical indication mean a selection of patients who likely will have less postoperative disabilities. Living with a severe neurological impairment may appear more acceptable in some cultures, and inhumane in others. A recent review anyway concluded that the vast majority of operated patients do not regret having undergone surgery 14).

The natural history of middle cerebral artery occlusion MCA occlusion has become increasingly important since the surgical option of EC/IC bypass surgery has been available.

The clinical course of 24 patients with angiographically-demonstrated occlusion of the MCA artery was reviewed. Eight patients presented with a major disabling stroke and five of these died during the acute phase of this ischemic event. The remaining 19 patients were followed for a mean of 54.2 months. There were five deaths in follow-up and two of these were due to subsequent strokes. Fourteen patients manifested a benign course: one of these had a further minor stroke and four had TIAs. Altogether, 3 strokes occurred during the follow-up period (2 fatal, 1 minor) and all were in the territory of the artery known to be occluded. Of those patients who survived their presenting ischemic event, 12 (63%) remained completely functional in terms of activities of daily living. MCA occlusion does not necessarily carry a poor prognosis with medial therapy alone and the role of bypass surgery hopefully will be clarified by the ongoing clinically randomized trial 15).

Case series

Encephaloduroarteriosynangiosis (EDAS) as a form of indirect revascularization has been recently proposed as a potentially promising alternative for patients with intracranial atherosclerotic disease (ICAD). The object of a study was to compare the prognostic roles between isolated EDAS and medical therapy in patients with atherosclerotic middle cerebral artery occlusion (MCAO).

From January 2014 to June 2017, 125 patients with atherosclerotic MCAO were enrolled in this prospective nonrandomized controlled cohort study. Patients who underwent EDAS (n = 60) were compared with those treated medically (n = 65). Early and late adverse events and functional outcomes including memory ability were compared between groups.

During 23.7 months of mean follow-up, rates of adverse events, including ischemic events in the territory of the qualifying middle cerebral artery (MCA), and death from any causes, were not significantly different in patients treated with EDAS and with medical therapy (6.7% vs. 12.3%; p=0.285). Landmark analyses revealed that at initial 6-month follow-up, there was no significant difference for adverse event rates, while the opposite finding was demonstrated for the subsequent period (EDAS 1/57 [1.7%] vs. medical management 7/64 [10.9%]; p=0.024). And the P value for the interaction between time (first 6 months vs. subsequent period) was 0.044. No significant differences were found with the respect to neural function status and cognitive ability.

In the long-term, isolated EDAS can be considered effective and safe for patients with atherosclerotic MCAO, whereas it may need additional medical therapy support in the short-term 16).

Case reports

A 69-year-old with right hemiparesis and global aphasia. Perfusion computed tomography imaging revealed ischemic penumbra in the middle cerebral artery territory. Angiography showed left middle cerebral artery occlusion. Mechanical thrombectomy with one pass was performed, and successful recanalization was obtained. Embolic material was retrieved; it contained tumor fragments with atypical keratinizing squamous cell carcinoma. Contrast computed tomography imaging indicated tumor invasion into the superior vena cava, and contrast transcranial Doppler indicated the presence of a right-to-left shunt after the Valsalva maneuver. They diagnosed the patient with acute ischemic stroke of large vessel occlusion due to venous invasion of esophageal carcinoma via a right-to-left shunt. This is the first case of embolic occlusion resulting from an extracardiac tumor via a right-to-left shunt. Contrast transcranial Doppler potentially detects right-to-left shunts in patients who cannot undergo transesophageal echocardiography 17).

References

1)

Frank JI. Large hemispheric infarction, deterioration, and intracranial pressure. Neurology. 1995;45(7):1286–1290.
2) , 9)

Schwab S, Aschoff A, Spranger M, Albert F, Hacke W. The value of intracranial pressure monitoring in acute hemispheric stroke. Neurology. 1996;47(2):393–398.
3)

del Zoppo GJ, Mabuchi T. Cerebral microvessel responses to focal ischemia. Journal of Cerebral Blood Flow & Metabolism. 2003;23(8):879–894.
4)

Lam WWM, Leung TWH, Chu WCW, Yeung DTK, Wong LKS, Poon WS. Early computed tomography features in extensive middle cerebral artery territory infarct: prediction of survival. Journal of Neurology, Neurosurgery & Psychiatry. 2005;76(3):354–357.
5)

Hofmeijer J, Algra A, Kappelle LJ, van der Worp HB. Predictors of life-threatening brain edema in middle cerebral artery infarction. Cerebrovascular Diseases. 2008;25(1-2):176–184.
6)

Krieger DW, Demchuk AM, Kasner SE, Jauss M, Hantson L. Early clinical and radiological predictors of fatal brain swelling in ischemic stroke. Stroke. 1999;30(2):287–292.
7)

Kasner SE, Demchuk AM, Berrouschot J, et al. Predictors of fatal brain edema in massive hemispheric ischemic stroke. Stroke. 2001;32(9):2117–2123.
8)

Poca MA, Benejam B, Sahuquillo J, et al. Monitoring intracranial pressure in patients with malignant middle cerebral artery infarction: is it useful? Journal of Neurosurgery. 2010;112(3):648–657.
10)

Carhuapoma JR, Qureshi AI, Bhardwaj A, Williams MA. Interhemispheric intracranial pressure gradients in massive cerebral infarction. Journal of Neurosurgical Anesthesiology. 2002;14(4):299–303.
11) , 13)

Hacke W, Schwab S, Horn M, Spranger M, de Georgia M, von Kummer R. ‘Malignant’ middle cerebral artery territory infarction: clinical course and prognostic signs. Archives of Neurology. 1996;53(4):309–315.
12)

Wijdicks EFM, Diringer MN. Middle cerebral artery territory infarction and early brain swelling: progression and effect of age on outcome. Mayo Clinic Proceedings. 1998;73(9):829–836.
14)

Rahme R, Zuccarello M, Kleindorfer D, et al. Decompressive hemicraniectomy for malignant middle cerebral artery territory infarction: is lifeworth living? Journal of Neurosurgery. 2012;117(4):749–754.
15)

Moulin DE, Lo R, Chiang J, Barnett HJ. Prognosis in middle cerebral artery occlusion. Stroke. 1985 Mar-Apr;16(2):282-4. PubMed PMID: 3975967.
16)

Zhang Q, Li Y, Tong H, Wu X, Wang Y, Ge W, He C, Liu R, Yu S. Comparison of therapeutic efficacy between isolated encephaloduroarteriosynangiosis and medical treatment in patients with atherosclerotic middle cerebral artery occlusion. World Neurosurg. 2018 Jun 20. pii: S1878-8750(18)31272-5. doi: 10.1016/j.wneu.2018.06.057. [Epub ahead of print] PubMed PMID: 29935318.
17)

Araki S, Maekawa K, Kobayashi K, Sano T, Yabana T, Shibata M, Miya F. Tumor Embolism Through Right-to-Left Shunt Due to Venous Invasion of Esophageal Carcinoma. J Stroke Cerebrovasc Dis. 2020 Sep 30;29(12):105352. doi: 10.1016/j.jstrokecerebrovasdis.2020.105352. Epub ahead of print. PMID: 33010722.

Anterior Inferior Cerebellar Artery Anomalies

Anterior Inferior Cerebellar Artery Anomalies

The anterior inferior cerebellar arteryposterior inferior cerebellar artery (AICAPICA) common trunk anomaly is reportedly one of the most common vessel variants in the posterior circulation 1).


A healthy 59-year-old male with a unilateral sporadic vestibular schwannoma.

The patient elected to undergo a translabyrinthine approach for resection of a vestibular schwannoma. An aberrant loop of AICA was encountered during the temporal bone dissection within the petrous part of the temporal bone.

The patient suffered a presumed ischemic insult resulting in a fluctuating ipsilateral facial paresis and atypical postoperative nystagmus.

MRI demonstrated an ischemic lesion in the vascular distribution of the right anterior-inferior cerebellar artery, including the lateral portion of the right cerebellar hemisphere, middle cerebellar peduncle, and bordering the right cranial nerve VII nucleus. His functional recovery was excellent, essentially identical to the anticipated course in an otherwise uncomplicated surgery.

This case highlights the irregular anatomy of the AICA as well as the importance of thorough neurological exams in the postsurgical lateral skull base patient 2).


Anomaly in which a segment of the anteroinferior cerebellar artery (AICA) is embedded in the dura or bone surrounding the subarcuate fossa, a small depression in the bone posterior to the internal acoustic meatus (IAM), through which the subarcuate artery enters the bone. This anomaly places the artery at risk in removing the posterior wall of the IAM.

An anomalous AICA having a segment that was embedded in the dura covering on the bone surrounding the subarcuate fossa was found during a microsurgical dissection course. The senior author (ALR) has observed this anomaly in four patients during surgery for acoustic neuromas and in three specimens in microsurgery dissection courses. To define the microsurgical anatomy of the anomalous artery further, the latex-injected specimen was dissected in a stepwise manner using x3 to x40 magnification.

The anomalous AICA described in this report bifurcated into a rostral trunk and a caudal trunk near the facial-vestibulocochlear nerve complex. The caudal trunk formed a sharp lateral loop that was embedded in the dura covering the subarcuate fossa. The involved trunk continued to supply the suboccipital area normally supplied by the posteroinferior cerebellar artery, which was hypoplastic. The dura surrounding the anomalous loop was opened, and the adjacent bone was removed to free the anomalous loop from the subarcuate fossa so that the artery could be displaced medially to remove the posterior wall of the IAM. Although it has been reported that the AICA may occasionally be adherent to the dura over the subarcuate fossa, this study is the first to demonstrate an AICA that is embedded in the dura and bone of the subarcuate fossa.

Mobilizing the AICA loop that is embedded in the subarcuate fossa posterior to the IAM places the involved AICA at significant risk in exposing the contents of the IAM 3).


Reports of hemifacial spasm (HFS) associated with AICA-PICA common trunk are very rare. In the present study, we describe methods of microvascular decompression (MVD) for HFS caused by AICA-PICA common trunk compression.

Among 159 patients who underwent MVD for HFS, 16 patients had compression of the root exit zone by the AICA-PICA common trunk anomaly. The types of compression were classified into 2 groups: common trunk artery compression group and branching vessel compression group.

The common trunk artery compression group consisted of 11 patients (69%), and the branching vessel compression group consisted of 5 patients (31%). The rostral branch (feeding the original AICA territory) coursed between the seventh and eighth cranial nerves in 5 patients, and in 13 patients (81%), the offending vessel harbored perforators around the root exit zone. Among 16 patients, 14 (87.5%) required interposition of the common trunk or the branching vessel, and in 2 patients, decompression was completed by the transposition method. Fifteen patients experienced sufficient results, and 1 had severe residual spasm. Transient facial palsy developed in 2 patients. No patients encountered recurrence.

Reports concerning decompression methods of AICA-PICA common trunk anomaly are very rare. The tortuosity of the common trunk and perforators from the offending vessel make the usual repositioning of the offending artery much more difficult, and adequate decompression techniques are required for successful MVD 4).

References

1)

Shimano H, Kondo A, Yasuda S, Inoue H, Morioka J, Miwa H, Kawakami O, Murao K. Significance of Anomalous Anterior Inferior Cerebellar Artery-Posterior Inferior Cerebellar Artery Common Trunk Compression in Microvascular Decompression for Hemifacial Spasm. World Neurosurg. 2016 Aug;92:15-22. doi: 10.1016/j.wneu.2016.04.100. Epub 2016 May 4. PMID: 27155382.
2)

Bauer AM, Angster K, Schuman AD, Thompson BG, Telian SA. Aberrant AICA Injury During Translabyrinthine Approach. Otol Neurotol. 2020 Sep 28. doi: 10.1097/MAO.0000000000002826. Epub ahead of print. PMID: 33003181.
3)

Tanriover N, Rhoton AL Jr. The anteroinferior cerebellar artery embedded in the subarcuate fossa: a rare anomaly and its clinical significance. Neurosurgery. 2005 Aug;57(2):314-9; discussion 314-9. PubMed PMID: 16094161.
4)

Shimano H, Kondo A, Yasuda S, Inoue H, Morioka J, Miwa H, Kawakami O, Murao K. Significance of Anomalous Anterior Inferior Cerebellar Artery-Posterior Inferior Cerebellar Artery Common Trunk Compression in Microvascular Decompression for Hemifacial Spasm. World Neurosurg. 2016 Aug;92:15-22. doi: 10.1016/j.wneu.2016.04.100. PubMed PMID: 27155382.
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