Книги по МРТ КТ на английском языке / Neurovascular anatomy in interventional neuroradiology Krings et al 2015

10.3 Clinical Impact

Treatment of aneurysms associated with this variation will vary depending on the type of infraoptic course. In type 1, the presence of both an infraoptic A1 and a supraoptic A1 provides an additional access route for endovascular intervention. In type 2 configurations (with infraoptic A1), the aneurysms may be approached surgically via an anterior interhemispheric or subfrontal approach if endovascular options are not deemed possible. In cases with a proximal aneurysm of the infraoptic A1, however, the aneurysm may be obscured by the optic nerve during craniotomy. Because these types of aneurysms are usually in close proximity to the cavernous sinuses and the cranial nerves, they may be more di cult to treat surgically. Proximal control of the parent vessel may require an extended skull-base approach. In type 3, the absence of contralateral A1 limits the time allowed for temporary clipping. These considerations highlight why in our practice endovascular options are the method of first choice in patients presenting with an aneurysm and this peculiar variation.

including inherited connective tissue disorders, intrinsic structural factors such as medial defects, and acquired factors such as hypertension and hemodynamic stress. In 10% of cases, tumors (prolactinomas and craniopharyngiomas) have been present. Rarely, an infraoptic ACA is associated with congenital cranial abnormalities, such as abnormal gyral segmentation and craniofacial anomalies ( Fig. 10.3; Fig. 10.4; Fig. 10.5).

Pearls and Pitfalls

●An infraoptic segment of the A1 should be diagnosed if the A1 arises from the ICA at the level of the ophthalmic artery and if the vessel courses underneath the optic nerve.

●Most infraoptic ACAs are right-sided, but they can occur bilaterally.

●Proximal A1 aneurysms may be obscured during surgery by the optic nerve in patients with an infraoptic course of the A1.

10.4 Additional Information and

Cases

Many anatomic variations associated with an infraoptic ACA have been described in the literature. They include association with a fused pericallosal artery, agenesis of the contralateral ICA, ectopic origin of the sylvian artery, azygous A2, carotid– vertebrobasilar artery anastomoses, plexiform AcomA, ophthalmic artery arising from the middle meningeal artery, and absent ACA associated with coarctation or Moyamoya. The infraoptic A1 s are frequently associated with intracranial aneurysms, according to the literature, in more than 50% of cases. Approximately two-thirds of the aneurysms are seen in the AComA. The pathogenesis of the aneurysms involves several factors,

Further Reading

[1]Chakraborty S, Fanning NF, Lee SK, ter Brugge KG. Bilateral infraoptic origin of anterior cerebral arteries: a rare anomaly and its embryological and clinical significance. Interv Neuroradiol 2006; 12: 155–159

[2]Lasjaunias P, Berenstein A, ter Brugge KG. Surgical Neuroangiography. Vol. 1. 2nd ed. Berlin: Springer; 2006

[3]Mercier P, Velut S, Fournier D et al. A rare embryologic variation: carotid-an- terior cerebral artery anastomosis or infraoptic course of the anterior cerebral artery. Surg Radiol Anat 1989; 11: 73–77

[4]Spinnato S, Pasqualin A, Chio F, Da Pian R. Infraoptic course of the anterior cerebral artery associated with an anterior communicating artery aneurysm: anatomic case report and embryological considerations. Neurosurgery 1999; 44: 1315–1319

[5]Wong ST, Yuen SC, Fok KF, Yam KY, Fong D. Infraoptic anterior cerebral artery: review, report of two cases and an anatomical classification. Acta Neurochir (Wien) 2008; 150: 1087–1096

11.1 Case Description

11.1.1 Clinical Presentation

A 37-year-old woman with long-standing chronic hydrocephalus presented with an incidental unruptured anterior communicating artery (AComA) aneurysm.

11.1.2 Radiologic Studies

See Fig. 11.1.

11.1.3 Diagnosis

AComA aneurysm.

11.2 Anatomy

The most widely used classification of anterior cerebral artery (ACA) anatomy to date is the one proposed in 1938 by Fischer. It defines five segments: A1, the precommunicating segment; A2, the segment that runs below the genu of the corpus callosum; A3, the segment that runs around the genu of the corpus callosum; and A4 and A5, which are considered the terminal portions of the ACA. Given that it has become common language in the neurovascular anatomy, this nomenclature is used in this section.

The right and left A1 segments join to form the AComA in the midline in the lamina terminalis region, above the optic chiasm (70%) or, less frequently, above the cisternal segment of the optic nerves (30%). The “classic” anatomy, in which two equalsized A1 segments form the AComA, is seen in only 20% of cases. Most commonly, one A1 segment will be dominant and bifurcate into the two A2 segments. In these cases, the AComA will be defined by the entry point of the hypoplastic A1. Complete absence of the A1 segment does not occur.

The AComA complex gives rise to small perforating vessels that are highly variable. Most commonly, these arteries will arise from the medial part of the AComA when the A1 segments are symmetrical, and ipsilateral to the dominant A1 when the segments are unequal. In cases of fenestrated or duplicated AComA, both limbs will have perforators arising from each limb. Three major groups of perforators have been described: the hypothalamic arteries that supply the lamina terminalis, the anterior hypothalamus, and the infundibulum of the pituitary; the chiasmal branches; and the subcallosal branches, which supply the rostrum and genu of the corpus callosum, the anterior cingulate gyrus, the septum pellucidum, and both columns of the fornix. The subcallosal artery is usually the largest, and often it is a single branch, whereas the other groups of perforators often consist of multiple small branches.

The anatomy of the medial lenticulostriate arteries arising from the ACA and of the recurrent artery of Heubner is discussed in Case 14. Multiple variations of the AcomA complex and its adjacent vessels can be identified.

Fig. 11.1 Axial T2-weighted MRI (a) shows dilated ventricles and a prominent flow void in the AComA region (white arrow). Time-of-flight magnetic resonance angiography (b) and left internal carotid artery (ICA) angiogram in working projection (c) reveal a broad-necked AComA aneurysm. Plain radiography (d) and simultaneous bilateral carotid injections (d) after X-stenting and coiling show complete occlusion of the aneurysm. The decision to perform an X-stent-assisted coiling was made to preserve the patency of the AComA.

11.2.1 A1 Segment Fenestration

Fenestrations of the A1 segment are rare, with an estimated prevalence of 0 to 4% in anatomic studies and less than 0.1% in angiographic studies ( Fig. 11.2). These fenestrations may be caused by the optic nerve coursing through the fenestration, which can be explained by the same considerations used to explain the infraoptic course of the A1, as outlined in the previous chapter; in most instances, though, a fenestration of the A1 segment is related to incomplete obliteration of anastomoses of a primitive vascular network. An association between A1 fenestrations and proximal A1 aneurysms has been proposed, but it is mostly based on isolated case reports.

11.2.2 AComA Fenestration

The AComA develops from a multichanneled vascular network during the embryologic stage that coalesces in various degrees by the time of birth. This process is responsible for the wide variety of AcomAs.

Fenestrations of the AComA are common, with large autopsy and surgical series reporting single, double, or even triple fenestrations of the AComA in up to 40% of specimens. The prevalence of these variations in imaging literature will vary, depending on the technique used. At this time, the gold standard is considered to be 3D rotational catheter angiography, given its highest spatial resolution and postprocessing capabilities. With this technique, variations can be seen in about 5% of cases. The

di erence from the surgical literature can be explained because in current practice, not all vessels are studied with 3D angiography, and competing flow from the contralateral A1 can preclude the opacification of smaller fenestrated limbs. In addition, in many fenestrations, bridging arteries are too thin (0.1–0.3 mm) and are beyond the spatial resolution of 3D angiography.

There is a proposed association between AComA fenestrations and aneurysms that is highlighted by the fact that about 8% of patients with AComA aneurysms harbor visible AComA fenestrations ( Fig. 11.3; Fig. 11.4).

proximal primitive olfactory artery does not occur, the ACA or some of the ACA branches may arise from this persistent embryonic vessel ( Fig. 11.5). The persistent primitive olfactory artery courses along the straight sulcus and makes a characteristic hairpin turn to give rise to the distal ACA. Angiography in these cases may demonstrate an absent recurrent artery of Heubner. The incidence of ruptured aneurysms in patients with a persistent primitive olfactory artery has been reported to be high.

11.2.3 Persistent Primitive Olfactory

Artery

A persistent primitive olfactory artery is a rare, but wellknown, variant of the proximal ACA, with an estimated prevalence of 0.14%. The ACA begins to develop as a secondary branch of the primitive olfactory artery at 5 weeks’ gestation. Normally, the primitive olfactory artery regresses and becomes the recurrent artery of Heubner. If the normal regression of the

11.3 Clinical Impact

The main e ect on the endovascular treatment that variations of the AComA anatomy have is in deciding the approach for the treatment of AComA aneurysms. Symmetric A1 segments may not tolerate two endovascular devices in them, so a bilateral approach with two femoral accesses should be considered. In addition, the angle in which the aneurysm arises from the AComA complex may make one side more favorable for endovascular approach than the other.

It is also important to be aware of the local arterial anatomy and the branches arising from this region. E orts should always be made to preserve the AcomA complex branches, as they supply highly eloquent brain regions. The operator should be familiar with the potential neurological syndromes related to ischemia from these territories ( Fig. 11.6; Fig. 11.7). Temporary occlusion with balloon catheters should be kept to a

minimum during balloon-assisted coiling, even if distal flow to the ACA is seen from the contralateral A1.

11.4 Additional Information and

Cases

See Fig. 11.8.

Pearls and Pitfalls

●The anatomy of the AComA complex region is highly variable. This can be explained by persistence of anastomotic channels from a primitive vascular network of this region.

●There are several small arteries that arise from the anterior communicating artery and supply highly eloquent brain tissue, the most prominent of which is the subcallosal artery.

●Fenestrations may be associated aneurysm formation.

Further Reading

[1]Aktüre E, Arat A, Niemann DB, Salamat MS, Başkaya MK. Bilateral A1 fenestrations: Report of two cases and literature review. Surg Neurol Int 2012; 3: 43

[2]Avci E, Fossett D, Aslan M, Attar A, Egemen N. Branches of the anterior cerebral artery near the anterior communicating artery complex: an anatomic study and surgical perspective. Neurol Med Chir (Tokyo) 2003; 43: 329–333, discussion 333

[3]de Gast AN, van Rooij WJ, Sluzewski M. Fenestrations of the anterior communicating artery: incidence on 3D angiography and relationship to aneurysms. AJNR Am J Neuroradiol 2008; 29: 296–298

[4]Dimmick SJ, Faulder KC. Fenestrated anterior cerebral artery with associated arterial anomalies. Case reports and literature review. Interv Neuroradiol 2008; 14: 441–445

[5]Dimmick SJ, Faulder KC. Normal variants of the cerebral circulation at multidetector CT angiography. Radiographics 2009; 29: 1027–1043

[6]Fischer E. Die Lageabweichungen der vorderen Hirnarterie im Gefäßbild. Zentralbl Neurochir 1938; 3: 300–313

[7]Hernesniemi J, Dashti R, Lehecka M et al. Microneurosurgical management of anterior communicating artery aneurysms. Surg Neurol 2008; 70: 8–28, discussion 29

[8]Kwon WK, Park KJ, Park DH, Kang SH. Ruptured saccular aneurysm arising from fenestrated proximal anterior cerebral artery: case report and literature review. J Korean Neurosurg Soc 2013; 53: 293–296

[9]Serizawa T, Saeki N, Yamaura A. Microsurgical anatomy and clinical significance of the anterior communicating artery and its perforating branches. Neurosurgery 1997; 40: 1211–1216, discussion 1216–1218

[10]van Rooij SB, van Rooij WJ, Sluzewski M, Sprengers ME. Fenestrations of intracranial arteries detected with 3D rotational angiography. AJNR Am J Neuroradiol 2009; 30: 1347–1350

12.1 Case Description

12.1.1 Clinical Presentation

A 54-year-old woman was investigated for recurrent migraines. Unenhanced computed tomography at an outside institution had revealed an aneurysm.

12.1.2 Radiographic Studies

See Fig. 12.1.

12.1.3 Diagnosis

Azygos anterior cerebral artery (ACA) with a callosomarginal bifurcation aneurysm.

12.2 Embryology and Anatomy

The azygos ACA is a relatively uncommon vascular anomaly, with a prevalence ranging between 0.2% and 4%. Embryologically, the azygos vessel appears to form via fusion of the A2 segment, which originates either from the medial branch of the olfactory artery at the 16-mm stage of embryogenesis (40 days of gestation) or from the continuation of the median artery in the corpus callosum at the 20–24-mm stage. According to the Baptista classification, the azygos ACA is type 1 when there is a single unpaired ACA, as in the present case description. In type 2, there are bihemispheric ACAs, one of which is dominant and

supplies both hemispheres. Finally, in type 3, there is an accessory ACA in the presence of a median artery that arises from the anterior communicating artery. Type 2 has an estimated prevalence of 2 to 7%. It can be di erentiated from the azygos ACA by the presence of a hypoplastic A2 segment. Its main clinical relevance is that occlusion of the dominant A2 segment will result in bilateral ACA territory infarcts. Type 3 has also been termed ACA trifurcation. The ACA trifurcation is defined by three A2 segments arising from the anterior communicating artery. It has an estimated prevalence of 2 to 13%. This normal variant may be explained by persistence and/or enlargement of the median callosal artery ( Fig. 12.2).

Azygos ACAs are associated with other malformations, including midline anomalies, such as corpus callosum agenesis, holoprosencephaly, hydranencephaly, and defects of septum pellucidum. There appears to be an association with arteriovenous malformations ( Fig. 12.3), saccular aneurysms, defects of olfactory bulbs and tracts, and polycystic kidney disease.

Among these, the presence of saccular aneurysms is the most significant association. The incidence of aneurysm formation ranges from 13 to 71% in azygos ACA. These aneurysms are usually located at distal bifurcations of the unpaired ACA, generally at the callosomarginal bifurcation. Augmentation of hemodynamic stress is implicated as one of the probable mechanisms in aneurysm formation; another possible factor is ectasia of the azygos vessel resulting from mural degenerative changes.