Double origin of the posterior inferior cerebellar artery

Double origin of the posterior inferior cerebellar artery

The posterior inferior cerebellar artery (PICA) frequently arises from the fenestrated segment of the intracranial vertebral artery (VA), and this common variation can be misinterpreted as or confused with a PICA of double origin. Rarely, a PICA of true double origin occurs when two branches of the PICA arise separately from the intracranial VA and fuse to form an arterial ring.

Uchino et al. discovered this rare variation incidentally while interpreting images of magnetic resonance angiography. This is the first report of MR angiographic findings of this rare variation 1).


For Lesley et al. double origin of the PICA is seen in 4.1% of patients with intracranial aneurysms and on 1.45% of catheter angiograms. The double origin of the PICA has an increased association with intracranial aneurysmal disease and may represent a risk factor for subsequent development of an intracranial aneurysm 2).


Posterior fossa arteriovenous malformations (AVMs), especially cerebellar arteriovenous malformations, are also not common. Consequently, the association of a Double origin of the posterior inferior cerebellar artery (DOPICA) with a cerebellar AVM is even rare.

Rodriguez-Calienes et al. presented a rare case of a pediatric cerebellar AVM supplied by a branch of a DOPICA which was treated endovascularly with NBCA. Total obliteration was achieved in the immediate controls and at 1-year follow-up.

Navigation through tortuous and long branches from a DOPICA is technically feasible. Although NBCA cure rates are relatively low, when the microcatheter can no longer navigate through the feeding artery, a correct dilution of NBCA with lipiodol can provide adequate penetration of this embolic agent, to obliterate the AVM nidus completely 3).


A cadaveric specimen was prepared for dissection. A far lateral craniotomy was performed on the right side. While exploring the right cerebellomedullary cistern, two separate origins of PICA were found from the vertebral artery (VA) as the caudal and rostral trunks that joined to form the distal PICA trunk at the tonsillomedullary segment. Microscopic and endoscopic illustrations are provided.

To the best of the authors’ knowledge, this is the first anatomic report on the DOPICA. Cadaveric illustration of this variant helps with understanding its anatomical relationship with adjacent neurovascular structures of the cerebellomedullary cistern including the perforating arteries and the lower cranial nerves 4).


Cho et al. demonstrated the first case of double origin of the posterior inferior cerebellar artery (PICA) with juxta-proximal fenestration of the caudal component, which was misunderstood as triple origin, combined with an unruptured middle cerebral artery aneurysm. The caudal component of the PICA originated from the atlanto-occipital portion and it was fenestrated shortly after origin. The cranial component originated from the intracranial vertebral artery and converged with the superior branch of the caudal component, and then met the inferior branch of the caudal component distally 5).


Two cases of anatomical variation of the PICA that they have called its double origin, one of which gave rise to an aneurysm. The first patient was a 36-year-old man who presented with a subarachnoid hemorrhage related to the rupture of a PICA aneurysm. The aneurysm was treated by the endovascular route. Selective and super selective studies showed that the PICA origin was low on the fourth segment of the vertebral artery (VA). The aneurysm was located on an anastomosis between the PICA and a small upper arterial branch originating from the VA. Embolization was performed through the small branch with no problem, but a lateral medullary infarct followed, probably due to occlusion of the perforating vessels. The same anatomical variation was incidentally discovered in the second patient. To the authors’ knowledge, neither this anatomical variation of the PICA nor the aneurysm’s topography has been previously described angiographically. This highlights the role of angiography in pretreatment evaluation of aneurysms especially when perforating vessels or small accessory branches that are poorly visualized on angiographic studies are concerned, as in the territory of the PICA. Anatomy is sometimes unpredictable, and the surgeon must be very careful when confronted with these variations because they are potentially dangerous for endovascular treatment 6).


1)

Uchino A, Saito N, Ishihara S. Double Origin of the Posterior Inferior Cerebellar Artery Diagnosed by MR Angiography: A Report of Two Cases. Neuroradiol J. 2015 Apr;28(2):187-9. doi: 10.1177/1971400915576659. Epub 2015 Apr 13. PMID: 25923681; PMCID: PMC4757150.
2)

Lesley WS, Rajab MH, Case RS. Double origin of the posterior inferior cerebellar artery: association with intracranial aneurysm on catheter angiography. AJR Am J Roentgenol. 2007 Oct;189(4):893-7. doi: 10.2214/AJR.07.2453. PMID: 17885063.
3)

Rodriguez-Calienes A, Saal-Zapata G, De la Cruz J. Endovascular Treatment of an Arteriovenous Malformation Associated with a Double Origin of the Posterior Inferior Cerebellar Artery. Pediatr Neurosurg. 2021 Jul 8:1-5. doi: 10.1159/000517248. Epub ahead of print. PMID: 34237747.
4)

Meybodi AT, Moreira LB, Zhao X, Lawton MT, Preul MC. Double Origin of the Posterior Inferior Cerebellar Artery: Anatomic Case Report. World Neurosurg. 2019 Jan 3:S1878-8750(18)32950-4. doi: 10.1016/j.wneu.2018.12.127. Epub ahead of print. PMID: 30611945.
5)

Cho YD, Han MH, Lee JY. Double origin of the posterior inferior cerebellar artery with juxta-proximal fenestration of caudal component. Surg Radiol Anat. 2011 Apr;33(3):271-3. doi: 10.1007/s00276-010-0747-9. Epub 2010 Nov 24. PMID: 21107570.
6)

Pasco A, Thouveny F, Papon X, Tanguy JY, Mercier P, Caron-Poitreau C, Herbreteau D. Ruptured aneurysm on a double origin of the posterior inferior cerebellar artery: a pathological entity in an anatomical variation. Report of two cases and review of the literature. J Neurosurg. 2002 Jan;96(1):127-31. doi: 10.3171/jns.2002.96.1.0127. PMID: 11794593.

Malignant middle cerebral artery territory infarction

Malignant middle cerebral artery territory infarction

The malignant middle cerebral artery territory infarction is a distinct syndrome that occurs in up to 10% of stroke patients, 1) 2) which carries a mortality of up to 80% (mostly due to severe postischemic cerebral edema → increased ICP → herniation 3)

Patients usually present with findings of severe hemispheric stroke (hemiplegia, forced eye and head deviation) often with CT findings of major infarct within the first 12 hours. Most develop drowsiness shortly after admission. There is progressive deterioration during the first 2 days, and subsequent transtentorial herniation usually within 2–4 days of stroke. Fatalities are often associated with: severe drowsiness, dense hemiplegia, age > 45–50 yrs, 4) early parenchymal hypodensity involving > 50% of the MCA distribution on CT scan,23 midline shift > 8–10 mm, early sulci effacement, and hyperdense artery sign (p. 1354) 5) in MCA. Neurosurgeons may become involved in caring for these patients because aggressive therapies in these patients may reduce morbidity and mortality. Options include:

  1. conventional measures to control ICP (with or without ICP monitor): mortality is still high in this group and elevated ICP is not a common cause of initial neurologic deterioration in large hemispheric stroke

2. hemicraniectomy (decompressive craniectomy):

  1. ✖ to date, the following treatments have not improved outcome: agents to lyse clot, hyperventilationmannitol, or barbiturate coma.

In patients with severe middle cerebral artery (MCA), intracranial atherosclerotic disease (ICAD), the mechanism of stroke is multifactorial, but hemodynamic insufficiency plays a significant role. This finding is important in selecting a subgroup of patients who may benefit from revascularization 6).

see Malignant middle cerebral artery syndrome.

Malignant middle cerebral artery territory infarction diagnosis.

Malignant middle cerebral artery territory infarction treatment.

Malignant middle cerebral artery territory infarction outcome.

A case of a child with serological evidence of SARS-CoV-2 infection whose onset was a massive right cerebral artery ischemia that led to a malignant cerebral infarction. The patient underwent a life-saving decompressive hemicraniectomy, with good functional recovery, except for residual hemiplegia. During rehabilitation, the patient also developed a lower extremity peripheral nerve neuropathy, likely related to a long-Covid syndrome 7).


A 39-year-old woman in the 24th week of pregnancy who suffered a right malignant MCA infarction that eventually required DC. The patient delivered a healthy baby and underwent a second surgery for cranioplasty 7 months later. 8).


1)

Moulin DE, Lo R, Chiang J, et al. Prognosis in Middle Cerebral Artery Occlusion. Stroke. 1985;16:282–284
2) , 3)

Hacke W, Schwab S, Horn M, et al. Malignant Middle Cerebral Artery Territory Infarction: Clinical Course and Prognostic Signs. Arch Neurol. 1996; 53:309–315
4) , 5)

Wijdicks EFM, Diringer MN. Middle Cerebral Artery Territory Infarction and Early Brain Swelling: Progression and Effect of Age on Outcome. Mayo Clin Proc. 1998; 73:829–836
6)

Dubow JS, Salamon E, Greenberg E, Patsalides A. Mechanism of Acute Ischemic Stroke in Patients with Severe Middle Cerebral Artery Atherosclerotic Disease. J Stroke Cerebrovasc Dis. 2014 Jan 11. pii: S1052-3057(13)00425-4. doi: 10.1016/j.jstrokecerebrovasdis.2013.10.015. [Epub ahead of print] PubMed PMID: 24424333.
7)

Scala MR, Spennato P, Cicala D, Piccolo V, Varone A, Cinalli G. Malignant cerebral infarction associated with COVID-19 in a child. Childs Nerv Syst. 2021 Jun 26. doi: 10.1007/s00381-021-05273-x. Epub ahead of print. PMID: 34175976.
8)

Fernández García A, Jiménez Zapata HD, de Lera Alfonso MC, Sánchez Fernández C, Jiménez Arribas P, Rodríguez Arias CA. Decompressive Craniectomy in Pregnant Women. J Neurol Surg A Cent Eur Neurosurg. 2021 Jun 2. doi: 10.1055/s-0041-1726108. Epub ahead of print. PMID: 34077979.

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).


1)

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.
2)

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, https://doi.org/10.1016/j.inat.2021.101097. (https://www.sciencedirect.com/science/article/pii/S2214751921000098
3)

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.
4)

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
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